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Incidence of agonal respirations in sudden cardiac arrest.

STUDY OBJECTIVE: To discover the frequency of agonal respirations in cardiac arrest calls, the ways callers describe them, and discharge rates associated with agonal respirations. DESIGN: We reviewed taped recordings of calls reporting cardiac arrests and emergency medical technician and paramedic incident reports for 1991. Arrests after arrival of emergency medical services were excluded. SETTING: King County, Washington, excluding the city of Seattle. PARTICIPANTS: Four hundred forty-five persons with out-of-hospital cardiac arrests receiving emergency medical services. INTERVENTIONS: Telephone CPR, emergency medical technicians-defibrillation, and advanced life support by paramedics. MEASUREMENTS AND MAIN RESULTS: Any attempts at breathing described by callers were identified, as well as whether agonal respirations could be heard by dispatcher, emergency medical technicians, or paramedics. Agonal respirations occurred in 40% of 445 out-of-hospital cardiac arrests. Callers described agonal breathing in a variety of ways. Agonal respirations were present in 46% of arrests caused by cardiac etiology compared with 32% in other etiologies (P < .01). Fifty-five percent of witnessed arrests had agonal activity compared with 16% of unwitnessed arrests (P < .001). Agonal respirations occurred in 56% of arrests with a rhythm of ventricular fibrillation compared with 34% of cases with a nonventricular fibrillation rhythm (P < .001). Twenty-seven percent of patients with agonal respirations were discharged alive compared with 9% without them (P < .001). CONCLUSION: There is a high incidence of agonal activity associated with out-of-hospital cardiac arrest. Presence of agonal respirations is associated with increased survival. These findings have implications for public CPR training programs and emergency dispatcher telephone CPR programs.

Emergency Medical Services↗

Long term outcome after out-of-hospital cardiac arrest with physician staffed emergency medical services: the Utstein style applied to a midsized urban/suburban area.

OBJECTIVE: To test the effect of a physician staffed advanced cardiac life support (ALS) system on patient outcome following out-of-hospital cardiac arrest. DESIGN: Observational study. SETTING: Two tier basic life support (BLS) and physician staffed ALS services in the midsized urban/suburban area of Heidelberg, Germany. PATIENTS: All patients suffering out-of-hospital cardiac arrest of cardiac aetiology between January 1992 and December 1994 and who were covered by ALS services. INTERVENTIONS: Physician staffed ALS services. MAIN OUTCOME MEASURES: Return of spontaneous circulation, hospital discharge, and one year survival, according to the Utstein style. RESULTS: Of 330 000 inhabitants, 755 suffered from cardiac arrest covered by the Heidelberg ALS services. In 512 patients, cardiopulmonary resuscitation had been initiated. Of 338 patients with cardiac aetiology, return of spontaneous circulation was achieved in 164 patients (49%), 48 (14%) were discharged alive, and 40 (12%) were alive one year later; most of these patients showed good neurological outcome. Thus, 4.85 patients with cardiac aetiology were saved by the ALS services and discharged alive per 100 000 inhabitants a year. Ventricular fibrillation or tachycardia was detected in 106 patients (31%), other cardiac rhythms in 40 (12%), and asystole in 192 (57%). Hospital discharge rates (and one year survival) in these subgroups were 34.0% (29.2%), 12.5% (7.5%), and 3.6% (3.1%), respectively. Discharge rates increased if cardiac arrest was witnessed (bystander, 20.0%; BLS/ALS personnel, 21.4%; non-witnessed arrest, 3.3%; p < 0.01), and if the time period between the alarm and the arrival of the ALS unit was four minutes or less (</= 4 minutes, 30.6%; 4-8 minutes, 10.4%; > 8 minutes, 8. 1%; p < 0.001). In 69 patients with bystander witnessed cardiac arrest with ventricular fibrillation, the discharge rate was 37.7%; 21 patients were alive after one year. CONCLUSIONS: A two tier BLS and physician staffed ALS system is associated with good long term outcome of patients suffering from out-of-hospital cardiac arrest of cardiac aetiology in a midsized urban/suburban area. Further studies, however, are required to assess whether having a physician in the ALS unit is an independent determinant for improved long term outcome.

Aged↗

Early endothelial damage and leukocyte accumulation in piglet brains following cardiac arrest.

This study examined the early microvascular and neuronal consequences of cardiac arrest and resuscitation in piglets. We hypothesized that early morphological changes occur after cardiac arrest and reperfusion, and that these findings are partly caused by post-resuscitation hypertension. Three groups of normothermic piglets (37.5 degrees - 38.5 degrees C) were investigated: group 1, non-ischemic time controls; group 2, piglets undergoing 8 min of cardiac arrest by ventricular fibrillation, 6 min of cardiopulmonary resuscitation (CPR) and 4 h of reperfusion; and group 3, non-ischemic hypertensive controls, receiving 6 min of CPR after only 10 s of cardiac arrest followed by 4-h survival. Immediately following resuscitation, acute hypertension occurred with peak systolic pressure equal to 197 +/- 15 mm Hg usually lasting less than 10 min. In reacted vibratome sections, isolated foci of extravasated horseradish peroxidase were noted throughout the brain within surface cortical layers and around penetrating vessels in group 2. Stained plastic sections of leaky sites demonstrated variable degrees of tissue injury. While many sections were unremarkable except for luminal red blood cells and leukocytes, other specimens contained abnormal neurons, some appearing irreversibly injured. The number of vessels containing leukocytes was higher in group 2 than in controls (3.8 +/- 0.6% vs 1.4 +/- 0.4% of vessels, P < 0.05). Evidence for irreversible neuronal injury was only seen in group 2. Endothelial vacuolization was higher in groups 2 and 3 than in group 1 (P < 0.05). Ultrastructural examination of leaky sites identified mononuclear and polymorphonuclear leukocytes adhering to the endothelium of venules and capillaries only in group 2. The early appearance of luminal leukocytes in ischemic animals indicates that these cells may contribute to the genesis of ischemia reperfusion injury in this model. In both groups 2 and 3 endothelial cells demonstrated vacuolation and luminal discontinuities with evidence of perivascular astrocytic swelling. Widespread microvascular and neuronal damage is present as early as 4 h after cardiac arrest in infant piglets. Hypertension appears to play a role in the production of some of the endothelial changes.

Animals↗

Reversible myocardial depression in survivors of cardiac arrest.

Three patients under 40-years old who survived cardiac arrest due to ventricular fibrillation were originally diagnosed as having idiopathic dilated cardiomyopathy. Shortly after cardiac arrest, assessment of myocardial function revealed a globally dilated left ventricle in each patient with an estimated ejection fraction between 20% and 30%. Serial assessment of myocardial function, however, showed either normal or near-normal function by 2 weeks postevent. These findings suggest that myocardial stunning due to hypoperfusion during ventricular fibrillation or the effects of transthoracic shocks may result in profound, reversible myocardial depression in survivors of cardiac arrest. Serial evaluation of left ventricular function may be of value in selected survivors of cardiac arrest in order to evaluate time-dependent resolution of myocardial dysfunction and may prevent misdiagnosis of idiopathic dilated cardiomyopathy.

Adult↗

Gender modifies the influence of age on outcome after successfully resuscitated cardiac arrest: a retrospective cohort study.

Age is an important risk factor for mortality and unfavorable outcome after successfully resuscitated cardiac arrest. Other risk factors may interact with this relationship. We conducted the current study to quantify the influence of age on mortality and unfavorable neurologic outcome of patients surviving out-of-hospital cardiac arrest, and to determine the role of other confounding variables. This study was based on a cardiac arrest registry comprising all patients with witnessed out-of-hospital cardiac arrest of cardiac origin after successful resuscitation admitted to a department of emergency medicine between September 1991 and December 2004. We assessed the association between age and mortality and the degree of neurologic impairment, adjusting for multiple risk factors. We tested for interaction between age and all other risk factors with outcome. With each year of age the adjusted odds ratio for in-hospital death increased by 1.05 (95% confidence interval [CI], 1.04-1.07), and the adjusted odds ratio for an unfavorable neurologic outcome increased by 1.04 (95% CI, 1.03-1.06). Interaction between age and sex was present, and the analysis was stratified to sex. For men we found a steep risk increase for death and unfavorable outcome after being resuscitated from cardiac arrest, with the highest risk in the oldest age quartile. For women we observed only a slight risk increase for death and almost no risk increase for unfavorable outcome. Age is a strong independent risk factor for mortality and neurologic impairment after successfully resuscitated cardiac arrest. The risk increase with advancing age is much greater in men than in women. Therefore, in women, the influence of age on prognosis after cardiac arrest may not be very important, while in men it still plays an important role. This should be considered especially when treating successfully resuscitated women and discussing the prognosis with the medical team or the patient's family.

Adult↗

Cardiac arrest complicating acute myocardial infarction: predictability and prognosis.

Eleven percent of 905 consecutive patients with acute myocardial infarction admitted to the coronary care unit at Duke University Medical Center experienced cardiac arrest. Subgroups of patients at high and low risk for cardiac arrest were identified. Cardiac arrest was experienced by 17 percent of patients with signs of heart failure on admission but by only 3 percent of patients without diabetes mellitus, prior myocardial infarction or heart failure by history or on admission. Only 59 percent of patients with cardiac arrest survived hospitalization compared with 88 percent of those without cardiac arrest. Long-term survival for the 765 hospital survivors was significantly greater in the group without than in the group with arrest at each yearly interval from 1 through 5 years; the 2 year survival rate was 50 and 77 percent, respectively, in these two groups. Many of the deaths among the hospital survivors occurred in patients with signs of heart failure during hospitalization. Among 668 hospital survivors who had mild or no heart failure during hospitalization, cardiac arrest continued to be a significant predictor of mortality. The mode of death among hospital survivors did not differ in the groups with and without cardiac arrest; for example, the incidence rate of sudden death in the two groups was 44 and 37 per cent, respectively. In light of recent reports suggesting that the prophylactic use of antiarrhythmic agents can virtually eliminate virtually fibrillation during the hospital phase of acute myocardial infarction, we contend that such use may substantially reduce both long-term and hospital mortality after acute myocardial infarction.

Female↗

Minimal changes of TNF-alpha and MCP-1 expression in blood serum of rats subjected to experimental cardiac arrest.

UNLABELLED: The elucidation of various aspects of the pathomechanism of experimental cardiac arrest may contribute valuable information for the treatment of cardiac arrests in humans. The model of clinical death in rats introduced by Korpatchev et al. was used. An analysis of expression in the blood serum of TNF-alpha and of MCP-1 was performed as a contribution to this problem. The studied groups included rats 24, 48 hours and 14 days after experimental cardiac arrest. RESULTS: The level of serum TNF-alpha in all studied animal groups remained unchanged after global cerebral ischemia. MCP-1 expression was decreased only in the group of rats - two weeks after the cardiac arrest. CONCLUSION: The obtained results indicate that proinflammatory cytokines do not play a key role in the development of delayed neurodegeneration after cardiac arrest. Thus it is not so much the immunological reaction, but a neuroexcitatory mechanism that plays a decisive role in the delayed neuronal death.

Animals↗

Characteristics and outcome among patients having out of hospital cardiac arrest at home compared with elsewhere.

OBJECTIVE: To describe the characteristics and outcome of patients who have a cardiac arrest at home compared with elsewhere out of hospital. PATIENTS: Subjects were patients included in the Swedish cardiac arrest registry between 1990 and 1999. The registry covers about 60% of all ambulance organisations in Sweden. METHODS: The study sample comprised patients reached by the ambulance crew and in whom resuscitation was attempted out of hospital. There was no age limit. Crew witnessed cases were excluded. The patients were divided into two groups: cardiac arrest at home and cardiac arrest elsewhere. RESULTS: Among a study population of 24 630 patients the event took place at home in 16 150 (65.5%). Those in whom the arrest took place at home differed from the remainder in that they were older, were more often women, less often had a witnessed cardiac arrest, were less often exposed to bystander cardiopulmonary resuscitation (CPR), were less often found in ventricular fibrillation, and had a longer interval between collapse and call for ambulance, arrival of ambulance, start of CPR, and first defibrillation. Of patients in whom the arrest took place at home, 11.3% were admitted to hospital alive, v 19.4% in the elsewhere group (p < 0.0001); corresponding figures for survival after one month were 1.7% v 6.2% (p < 0.0001). The adjusted odds ratio for survival after one month (at home v not at home; considering age, sex, initial arrhythmia, bystander CPR, aetiology, and whether the arrest was witnessed) was 0.40 (95% confidence interval 0.33 to 0.49; p < 0.0001). CONCLUSIONS: Sixty five per cent of out of hospital cardiac arrests in Sweden occur at home. The patients differed greatly from those with out of hospital cardiac arrests elsewhere, and fewer than 2% were alive after one month. Having an arrest at home was a strong independent predictor of adverse outcome. Further research is needed to identify the reasons for this.

Adolescent↗

Causes and prognosis of cardiac arrest in a population admitted to a general hospital; a diagnostic and therapeutic problem.

BACKGROUND: The purpose of this study was to determine the causes and the prognosis of consecutive patients resuscitated from cardiac arrest occurring in a general hospital. We assessed 28 females and 94 males (aged 13-82 years) who were resuscitated from cardiac arrest not attributable to acute myocardial infarction. Ventricular fibrillation (VF) was documented in 97. Non-cardiac causes were excluded. Non-invasive studies (24 h Holter monitoring, 2D echocardiogram, signal-averaged ECG, exercise testing, magnetic resonance imaging) and invasive studies (right and left ventricular angiography, coronary angiography and complete electrophysiologic study (EPS) were performed. RESULTS: An underlying cardiac disease was found in 107 patients (88%). Patients were followed for a period ranging from 6 months to 10 years (mean 4+/-5 years). Several causes for cardiac arrest were identified and treated specifically. The prognosis was variable. Among surviving patients the following causes of cardiac arrest were found: Wolff-Parkinson-White syndrome (n=2), rapid supraventricular tachycardia (n=6), acquired or congenital long QT syndrome (n=7), complete atrioventricular block (n=3), proarrhythmic effect of an antiarrhythmic drug (n=5), vasospastic angina (normal coronary arteries) (n=5). Among ten patients with VF related to cardiac ischaemia two died suddenly. Ventricular tachycardia (VT) or VF was the main cause leading to resuscitation after cardiac arrest (n=64). The risk of recurrence of arrest is confirmed in the present study particularly in patients in whom VT/VF could not be suppressed by antiarrhythmic drug therapy (n=45) and in those where an ICD was not implanted (18 cardiac deaths (nine sudden cardiac deaths (SCD's)). The cause of cardiac arrest was not elucidated in 20 patients (16%). The prognosis of these patients differed according to the documentation of VF at the time of cardiac arrest: of those with documented VF (n=12), six patients died suddenly (one with an ICD); of those without documented VF (n=8), all are alive. CONCLUSION: To determine the precise cause of cardiac arrest was the first problem; the diagnosis of cardiac arrest clearly was erroneous in 8 of 122 patients (6.5%). In other patients, a ventricular tachyarrhythmia was identified as the cause for cardiac arrest in half of the population; the indication for an ICD is evident in this group. In 31% of patients with proven cardiac arrest, another arrhythmia requiring specific treatment was identified and ICD implantation was avoided; these patients had a survival of 92% at 3 years. In patients without an identified cause of cardiac arrest and negative EPS, the prognosis was unfavorable only in those with documented VF.

Adolescent↗

Suspended animation can allow survival without brain damage after traumatic exsanguination cardiac arrest of 60 minutes in dogs.

BACKGROUND: We have previously shown in dogs that exsanguination cardiac arrest of up to 120 minutes without trauma under profound hypothermia induced by aortic flush (suspended animation) can be survived without neurologic deficit. In the present study, the effects of major trauma (laparotomy, thoracotomy) are explored. This study is designed to better mimic the clinical scenario of an exsanguinating trauma victim, for whom suspended animation may buy time for resuscitative surgery and delayed resuscitation. METHODS: Fourteen dogs were exsanguinated over 5 minutes to cardiac arrest. Flush of saline at 2 degrees C into the femoral artery was initiated at 2 minutes of cardiac arrest and continued until a tympanic temperature of 10 degrees C was achieved. The dogs were then randomized into a control group without trauma (n = 6) or a trauma group (n = 8) that underwent a laparotomy and isolation of the spleen before hemorrhage and then, at the start of cardiac arrest, spleen transection and left thoracotomy. During cardiac arrest, splenectomy was performed. After 60 minutes of no-flow cardiac arrest, reperfusion with cardiopulmonary bypass was followed by intensive care to 72 hours. RESULTS: All 14 dogs survived to 72 hours with histologically normal brains. All control dogs were functionally neurologically intact. Four of eight trauma dogs were also functionally normal. Four had neurologic deficits, although three required prolonged mechanical ventilation because of airway edema and evidence of multiple organ failure. Blood loss from the chest and abdomen was variable and was associated with poor functional outcomes. CONCLUSION: Rapid induction of profound hypothermic suspended animation (tympanic temperature, 10 degrees C) can enable survival without brain damage after exsanguination cardiac arrest of 60 minutes even in the presence of trauma, although prolonged intensive care may be required. This technique may allow survival of exsanguinated trauma victims, who now have almost no chance of survival.

Abdominal Injuries↗

The efficacy of an ACLS training program for resuscitation from cardiac arrest in a rural community.

STUDY OBJECTIVE: To determine whether an advanced cardiac life support (ACLS) course in a rural hospital will improve resuscitation success from cardiac arrest. DESIGN: A retrospective case review of all patients in cardiac arrest during a 13-month period before and after the institution of an ACLS training program. SETTING: Emergency department of a 42-bed rural, community hospital in a community with no prehospital advanced life support or early defibrillation. PARTICIPANTS: All patients in cardiac arrest were entered into the data base. Twenty-nine patients were included in the pre-ACLS period and 35 in the post-ACLS period. There were no significant differences in age, gender, initial rhythm, comorbid diseases, witnessed versus unwitnessed arrest, or total arrest time in the patients in the pre-ACLS period compared with those in the post-ACLS period. INTERVENTION: ACLS provider training. MAIN RESULTS: Patients in cardiac arrest who had ventricular fibrillation/tachycardia as their initial rhythm had significant improvement in resuscitation success compared with patients in ventricular fibrillation/tachycardia in the pre-ACLS period (six of 15 versus none of nine, P < .05). Out-of-hospital cardiac arrest resuscitation was more successful in the post-ACLS period than in the pre-ACLS period (five of 30 versus none of 25, P < .05). Overall, seven of 35 patients (20%) were resuscitated successfully in the post-ACLS period, with two patients surviving to hospital discharge. This was not significantly different than the two of 29 patients (7%) resuscitated in the pre-ACLS period, with one patient surviving to discharge. CONCLUSION: The institution of an ACLS-provider course in a rural community hospital was associated with improvement in initial resuscitation for patients with ventricular fibrillation/tachycardia and out-of-hospital arrest.

Cardiopulmonary Resuscitation↗

Long-term outcomes of out-of-hospital cardiac arrest after successful early defibrillation.

BACKGROUND: Mortality after out-of-hospital cardiac arrest from ventricular fibrillation is high. Programs focusing on early defibrillation have improved the rate of survival to hospital discharge. We conducted a population-based analysis of the long-term outcome and quality of life of survivors. METHODS: All patients who had an out-of-hospital cardiac arrest between November 1990 and January 2001 who received early defibrillation for ventricular fibrillation in Olmsted County, Minnesota, were included. The survival rate was compared with that of an age-, sex-, and disease-matched (2:1) control population of residents who had not had an out-of-hospital cardiac arrest and with that of age- and sex-matched controls from the general U.S. population. The quality of life was assessed with use of the Medical Outcomes Study 36-item Short-Form General Health Survey (SF-36) and compared with U.S. population norms. RESULTS: Of 200 patients who presented with an out-of-hospital cardiac arrest with ventricular fibrillation, 145 (72 percent) survived to hospital admission (7 died in the emergency department) and 79 (40 percent) were neurologically intact (good overall capability or moderate overall disability) at discharge. The mean (+/-SD) length of follow-up was 4.8+/-3.0 years. Nineteen patients died after discharge from the hospital. The expected five-year survival rate (79 percent) was identical to that among age-, sex-, and disease-matched controls (P=0.68) but lower than that among the age- and sex-matched U.S. population (86 percent, P=0.02). Fifty patients completed SF-36 surveys at the end of follow-up, and the majority had a nearly normal quality of life, with the exception of reduced vitality. CONCLUSIONS: Long-term survival among patients who have undergone rapid defibrillation after out-of-hospital cardiac arrest is similar to that among age-, sex-, and disease-matched patients who did not have out-of-hospital cardiac arrest. The quality of life among the majority of survivors is similar to that of the general population.

Aged↗

[Comparative survey of cardiac arrests during anesthesia and surgery in the 1980 s and 1999 s].

A survey of unexpected cardiac arrests, excluding those associated with cardiac surgery, that had occurred during anesthesia and surgery in the period 1980-1999 was conducted. There was no significant difference between the number of such cardiac arrests that occurred in the 1980 s (29/36,159, 0.080%) and the number in the 1990 s (33/37,643, 0.088%). According to the classification by Keenan et al., there were 3 cases (0.0083%) in the 80 s and 4 cases (0.0106%) in the 90 s that occurred due to anesthetic management. Cardiac arrests due to surgery itself significantly decreased from 21 cases in the 80 s to 6 cases in the 90 s, probably due to proper treatment for massive bleeding, a decrease in the number of cases of anaphylactic shock, and the development of novel anesthetics. Conversely, cardiac arrests due to preoperative conditions of the patients significantly increased from 5 cases in the 80 s to 23 cases in the 90 s. This increase seems to be due to an increase in the number of severe and multiple injuries and an increase in complicated major surgery. The increase in number of cases due to preoperative conditions also depends on coronary spasm and cardiac conduction insufficiency. Taking into consideration the improvement in intraoperative monitoring and the development of novel anesthetics in the 90 s, greater efforts should be made by anesthesiologists to reduce the incidence of cardiac arrest due to anesthetic management, and preoperative evaluation of surgical patients needs to be reconsidered.

Anesthesia↗

Effects of U74006F on multifocal cerebral blood flow and metabolism after cardiac arrest in dogs.

Lipid peroxidation reactions during reperfusion after cardiac arrest may contribute to postischemic cerebral hypoperfusion, which in turn can contribute to permanent neurological dysfunction. We designed this study to determine whether the aminosteroid U74006F, a putative inhibitor of lipid peroxidation, mitigates cerebral multifocal hypoperfusion after cardiac arrest. We used our established dog model of ventricular fibrillation cardiac arrest (no blood flow) of 12.5 minutes, reperfusion by cardiopulmonary bypass of less than or equal to 5 minutes, and control of extracerebral variables during 4 hours postarrest. Cerebral blood flow was monitored by the stable xenon computed tomography method. Changes in cerebral oxygen consumption were obtained from mean blood flow values of coronal slices and the cerebral arteriovenous (sagittal sinus) oxygen content difference. A treatment group (n = 5) received U74006F starting with reperfusion (1.5 mg/kg i.a. plus 1.5 mg/kg i.v.) and three additional (graded) doses over 4 hours (total dose 4.5, 7.5, or 14.5 mg/kg). The U74006F-treated group showed the same postarrest transient hyperemia and protracted hypoperfusion in terms of global (computed tomography slice), regional, and local (multifocal) cerebral blood flow values and the same global cerebral oxygen consumption pattern as a concurrent control group (n = 5). At 1-4 hours postarrest, in both groups there was mismatching of global cerebral oxygen consumption, which reached baseline values, in relation to global cerebral blood flow and oxygen delivery, which remained at 50% of baseline. We conclude that treatment with U74006F after prolonged cardiac arrest causes no deleterious side effects and does not seem to alter multifocal postarrest cerebral blood flow and oxygen consumption.

Animals↗

Effect of ventilation on resuscitation in an animal model of cardiac arrest.

BACKGROUND: The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. METHODS AND RESULTS: Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of > 80 mm Hg for > 5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P < .05) lower mean arterial PO2 (38 +/- 17 mm Hg compared with 216 +/- 104 mm Hg) and higher PCO2 (62 +/- 16 mm Hg compared with 35 +/- 8 mm Hg), lower mixed venous PO2 (15 +/- 7 mm Hg compared with 60 +/- 7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P < .002). CONCLUSIONS: In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.

Animals↗

Detoxification with hemabsorption after cardiac arrest does not improve neurologic recovery. Review and outcome study in dogs.

We and others hypothesized that noxious substances released after prolonged cardiac arrest from malfunctioning liver, kidneys, or intestine (e.g. bacterial toxins, aromatic amino acids), might hamper recovery of the brain. The highly detoxifying effect of hemabsorption (i.e. hemoperfusion) with microencapsulated activated carbon has been demonstrated in other diseases. We used our dog model of ventricular fibrillation cardiac arrest of 15 min (n = 2 x 4) or 12.5 min (n = 2 x 6), reversed by brief (high flow) cardiopulmonary bypass (CPB). In half of the dogs in each insult group, a charcoal filter (HemoKart) was inserted into the circuit of CPB at low flow, from start of reperfusion to 4 h. Intermittent positive pressure ventilation was to 20 h and intensive care to 96 h after cardiac arrest. Bacterial blood cultures were positive in most of the dogs in both groups 30 min to 20 h after cardiac arrest (but not later) and were uninfluenced by hemabsorption. In the control groups to 4 h after cardiac arrest, serum levels of potentially injurious aromatic amino acids (e.g. phenylalanine, tyrosine) and of branched-chain/aromatic amino acid ratios, remained unchanged. From 12 to 48 h after cardiac arrest, aromatic amino acid levels increased (worsened). The branched-chain/aromatic amino acid ratios changed accordingly in the opposite direction. In the hemabsorption groups to 4 h after cardiac arrest, all amino acid levels were reduced, aromatic amino acids more so than branched-chain amino acids, thus increasing (improving) the ratio, compared with controls (P < 0.01). There was no group difference after discontinuance of hemabsorption at 4 h. Outcome in terms of overall performance categories and neurologic deficit scores from 24 to 96 h and brain histopathologic damage scores 96 h after cardiac arrest, were not significantly different between groups. The lack of a beneficial outcome effect of hemabsorption to 4 h after cardiac arrest does not support the self-intoxication hypothesis. The amino acid levels later after cardiac arrest suggest that more prolonged hemabsorption and more encompassing detoxification treatments, such as plasma phoresis or total body blood washout, might be evaluated.

Amino Acids↗

Myocardial dysfunction after resuscitation from cardiac arrest: an example of global myocardial stunning.

OBJECTIVES: This study investigated the effect of prolonged cardiac arrest and subsequent cardiopulmonary resuscitation on left ventricular systolic and diastolic function. BACKGROUND: Cardiac arrest from ventricular fibrillation results in cessation of forward blood flow, including myocardial blood flow. During cardiopulmonary resuscitation, myocardial blood flow remains suboptimal. Once the heart is defibrillated and successful resuscitation achieved, reversible myocardial dysfunction, or "stunning," may occur. The magnitude and time course of myocardial stunning from cardiac arrest is unknown. METHODS: Twenty-eight domestic swine (26 +/- 1 kg) were studied with both invasive and noninvasive measurements of ventricular function before and after 10 or 15 min of untreated cardiac arrest. Contrast left ventriculograms, ventricular pressures, cardiac output, isovolumetric relaxation time (tau) and transthoracic Doppler-echocardiographic studies were obtained. RESULTS: Twenty-three of 28 animals were successfully resuscitated and postresuscitation data obtained. Left ventricular ejection fraction showed a significant reduction 30 min after resuscitation (p < 0.05). Regional wall motion analysis revealed diffuse, global left ventricular systolic dysfunction. Left ventricular end-diastolic pressure increased significantly in the postresuscitation period (p < 0.05). Isovolumetric relaxation time (tau) was significantly increased over baseline by 2 h after resuscitation (p < 0.05). Similar findings were noted with the Doppler-echocardiographic analysis, including a reduction in fractional shortening (p < 0.05), a reduction in mitral valve deceleration time (p < 0.05) and an increase in left ventricular isovolumetric relaxation time at 5 h after resuscitation (p < 0.05> By 24 h, these invasive and noninvasive variables of systolic and diastolic left ventricular function had begun to improve. At 48 h, all measures of left ventricular function had returned to baseline levels. CONCLUSIONS: Myocardial systolic and diastolic dysfunction is severe after 10 to 15 min of untreated cardiac arrest and successful resuscitation. Full recovery of this postresuscitation myocardial stunning is seen by 48 h in this experimental model of ventricular fibrillation cardiac arrest.

Animals↗

Regional changes in glial cell line-derived neurotrophic factor after cardiac arrest and hypothermia in rats.

Hypothermia after resuscitation from cardiac arrest reduces functional and histological brain injury. Stimulation of neurotrophic factors may contribute to the beneficial effects of hypothermia. This study examined the effects of cardiac arrest and induced hypothermia on regional levels of glial cell line-derived neurotrophic factor (GDNF) over the first 24 h after rat cardiac arrest. Hypothermia increased GDNF in hippocampus at 6 h, but did not prevent a subsequent decline in hippocampal GDNF. In contrast, hypothermia prevented early increases in cortical levels of GDNF at 3 and 6 h. Cerebellar GDNF increased slightly over 24 h in hypothermia-treated rats, but brainstem levels of GDNF did not change in response to cardiac arrest or hypothermia. These results suggest that temperature after resuscitation produces regionally specific changes of GNDF levels in brain.

Animals↗