Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D01401 (CPR)
1,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Defibrillation after prolonged ventricular fibrillation (VF) is frequently followed by asystole or electromechanical dissociation (EMD) which are usually fatal. We studied the effects of glucagon, a known inotropic and chronotropic agent, during 19 episodes of postcountershock asystole/EMD in nine dogs. Systolic and diastolic aortic (Ao), left ventricular, pulmonary arterial, and right atrial (RA) pressures were recorded as was the instantaneous Ao-RA difference (coronary perfusion pressure) and coronary sinus blood flow (CSF) during closed-chest CPR. VF was induced electrically; 2 min later, a 400-J transthoracic shock was given. Countershock was always followed by asystole (n = 12) or EMD (n = 7). Conventional closed-chest CPR with a mechanical device was begun 30 to 60 sec after countershock and continued for 2 to 3 min. If a perfusing rhythm did not occur, glucagon (1 mg) was given iv and CPR continued for 2 to 3 min more. Glucagon had no significant effect on intravascular pressures, the coronary perfusion gradient, or CSF when compared to CPR alone. However, in 14 or 19 postcountershock episodes unresponsive to CPR alone, glucagon restored effective spontaneous circulation, i.e., successful cardiac resuscitation, due to its effects on the intrinsic pacemaker discharge rate. Glucagon has been previously shown to stimulate myocardial adenyl cyclase via nonadrenergic mechanisms. We conclude that when postcountershock asystole/EMD occurs, glucagon has a direct and favorable effect on cardiac resuscitation outcome due to its effects on pacemaker discharge rate which is not mediated by changes in myocardial blood flow or coronary perfusion pressure.
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PMID:Postcountershock pulseless rhythms: hemodynamic effects of glucagon in a canine model. 356 24

Ventricular fibrillation (VF) cardiac arrest of more than ten minutes can be survived by cerebral neurons, but restoration of spontaneous circulation (ROSC) by external CPR is unreliable. Cardiopulmonary bypass (CPB) permits control of pressure, flow, oxygenation, temperature, and composition of blood. After 12 1/2 minutes of normothermic VF cardiac arrest, CPB was used as a research tool for reperfusion and assisted circulation for two hours in ten dogs without thoracotomy, with plasma substitute priming, and without preceding CPR (a deliberately nonclinical scenario). Recovery was compared with that in ten control dogs in which standard CPR with advanced life support (ALS) for up to 30 minutes was used to achieve ROSC. Both groups subsequently had blood pressure, blood gases, ventilation, and other parameters controlled for 20 hours, and intensive therapy to 72 hours. CPB achieved ROSC more successfully (ten of ten vs six of ten controls) (P less than .05), and more rapidly, with fewer defibrillation attempts and with less epinephrine (P less than .05). CPB improved 72-hour survival (seven of ten vs two of ten controls) (P = .025). Between two and 24 hours, of those with ROSC, intractable cardiogenic shock killed four of six control dogs (NS). CPB was followed by fewer arrhythmias. CPB increased recovery of consciousness (five of ten CPB vs zero of six controls with ROSC) (P = .037), but achieved neurologic normality in only one of ten. Cardiac arrest and CPB (without CPR) resulted in less myocardial morphologic damage than did standard CPR (P less than .025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiopulmonary bypass after prolonged cardiac arrest in dogs. 357 63

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)
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PMID:Cardiopulmonary bypass after cardiac arrest and prolonged closed-chest CPR in dogs. 357 64

Survival from cardiac arrest is higher when the collapse occurs outside the home. Of 781 patients collapsing at home, 101 (13%) survived to hospital discharge. This compared with 66 survivors among 248 (27%) patients arresting outside the home (P less than .001). Patients collapsing outside the home were younger and more frequently were men. Cardiac arrests outside the home were more often witnessed, more likely to have bystander CPR, less often preceded by symptoms, and the collapsing rhythm was more frequently ventricular fibrillation. Mean time to CPR was shorter. Multivariate logistic regression showed that the effect of location on survival was still statistically significant, although diminished, after adjusting for the above variables (P less than .01). We speculate that comorbidity, underlying etiology, and activity level may explain the remaining difference. Because 76% of arrests occur in the home, efforts to increase the frequency of bystander-CPR through targeted and dispatcher-assisted CPR programs are warranted.
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PMID:The location of collapse and its effect on survival from cardiac arrest. 359 34

The improvement in cerebral blood flow (CBF) during CPR after epinephrine administration has been attributed to epinephrine's alpha-adrenergic properties. Methoxamine, a pure alpha-1 agonist, has only been shown to be comparable to epinephrine in restoring circulation after cardiac arrest in a canine model. This study compares the effectiveness of equipotent doses of epinephrine and methoxamine in improving CBF during CPR after a prolonged cardiac arrest in a swine model. Twenty-five swine, weighing 15.9 to 28.2 kg, underwent instrumentation for regional CBF using tracer microspheres. CBF was determined during normal sinus rhythm. After 10 min of ventricular fibrillation, CPR was begun with a pneumatic compressor. CBF measurements were again made during CPR. After 3 min of CPR, the swine were randomized to receive 0.02 or 0.2 mg/kg epinephrine, 0.1, 1.0, or 10.0 mg/kg methoxamine. Five swine were allocated to each group. CBF measurements were determined after drug administration and compared using a Bonferroni multiple comparison procedure. A p-value less than .05 was considered statistically significant. This study demonstrated that, after a 10-min cardiac arrest, CBF was extremely low, averaging less than 7 ml/min X 100 g during external CPR. There were no clinically significant improvements in regional CBF after 0.02 mg/kg of epinephrine, or the two lowest doses of methoxamine. The addition of 10 mg/kg of methoxamine clinically improved blood flow only to the most caudal CNS structures, including the pons, medulla, and cervical spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Methoxamine versus epinephrine on regional cerebral blood flow during cardiopulmonary resuscitation. 359 56

Survival after out-of-hospital cardiac arrest is intimately related to the time from cardiovascular collapse to the initiation of CPR, or downtime. Furthermore, the reperfusion technique that optimizes coronary and cerebral blood flow after cardiac arrest may also be dependent on downtime. Peak blood lactate levels have been shown to be unchanged throughout resuscitation and predictive of downtime in dogs subjected to cardiopulmonary arrest and open cardiac massage. The purpose of this study was to determine the course of arterial lactate levels in dogs subjected to a fibrillatory cardiopulmonary arrest and conventional closed-chest CPR (CCPR). Fourteen dogs were subjected to five minutes of cardiopulmonary arrest and 30 minutes of CCPR. Resuscitation was performed according to a standardized protocol. Arterial lactic acid samples were collected at timed intervals throughout the experiment. Mean arterial lactic acid levels increased significantly with each sampling interval during 30 minutes of CCPR (overall P less than .05). In nine dogs successfully resuscitated, there were no significant differences in mean arterial lactic acid levels after the return of spontaneous circulation (ROSC). Open-chest resuscitation after five minutes of ventricular fibrillation in dogs results in peak lactic acid levels that do not change significantly once internal cardiac massage is initiated. In contrast, CCPR in similarly arrested dogs does not appear to provide adequate tissue oxygenation and/or perfusion to prevent continuous lactic acid accumulation.
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PMID:Lactic acidosis during closed-chest CPR in dogs. 368 90

The effectiveness of bystander CPR recently has been challenged. We undertook a ten-year retrospective review of our prehospital experience with witnessed cardiorespiratory arrest to ascertain save rates in patients receiving and not receiving CPR before paramedic advanced life support (ALS). Traumatic and poisoning arrests and children less than 18 years old were excluded. A total of 1,905 patients presenting to a paramedic system from November 1, 1973, to October 31, 1983, were bystander-witnessed arrests and attempted paramedic resuscitations. Four hundred five paramedic-witnessed arrests were excluded. One hundred eighty-two of 1,248 (14.6%) who had CPR initiated before paramedic ALS arrival were saves, compared to 38 of 252 (15%) who had no CPR initiated until paramedic arrival (P = NS). A save was defined as a patient discharged from the hospital. The respective save rates for coarse ventricular fibrillation were 148 of 628 (23.6%) (CPR before paramedic arrival) vs 35 of 151 (CPR delayed until paramedic arrival) (23.2%); electromechanical dissociation (EMD), 11 of 209 (5.3%) vs 0 of 38; asystole, 19 of 401 (4.7%) vs 3 of 61 (4.9%); and ventricular tachycardia, four of ten (40%) vs 0 of two. In this prehospital system, bystander/first responder CPR was found not to improve hospital discharge rates except in patients with initially documented rhythm of EMD.
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PMID:Bystander/first responder CPR: ten years experience in a paramedic system. 370 61

Since the implementation of a paramedic system in Seattle, yearly survival rates from out-of-hospital cardiac arrest due to ventricular fibrillation have averaged 25% without any significant increase over the years. Outcome for cardiac arrest associated with other rhythms has been poor: when asystole was the first rhythm recorded, only 1% of patients survived; when electromechanical dissociation was initially present, only 6% survived. For cases of electromechanical dissociation, neither the type of rhythm nor the rate appear to influence outcome. Survival from ventricular fibrillation can be improved by shortening the delay to initiation of CPR and to defibrillation. When outcome in 244 witnessed arrests was related to the times to beginning CPR and to initial defibrillation, mortality increased 3% each minute until CPR was begun and 4% a minute until the first shock was delivered. New strategies that minimize delays appear to have the greatest promise for improving survival after cardiac arrest.
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PMID:Considerations for improving survival from out-of-hospital cardiac arrest. 375 49

Myocardial and cerebral blood flow can be generated during cardiac arrest by techniques that manipulate intrathoracic pressure. Augmentation of intrathoracic pressure by high-pressure ventilation simultaneous with compression of the chest in dogs has been shown to produce higher flows to the heart and brain, but has limited usefulness because of the requirement for endotracheal intubation and complex devices. A system was developed that can produce high intrathoracic pressure without simultaneous ventilation by use of a pneumatically cycled vest placed around the thorax (vest cardiopulmonary resuscitation [CPR]). The system was first tested in a short-term study of the maximum achievable flows during arrest. Peak vest pressures up to 380 mm Hg were used on eight 21 to 30 kg dogs after induction of ventricular fibrillation and administration of epinephrine. Microsphere-determined myocardial blood flow was 108 +/- 17 ml/min/100 g (100 +/- 16% of prearrest flow) and cerebral flow was 51 +/- 12 ml/min/100 g (165 +/- 39% of prearrest). Severe lung or liver trauma was noted in three of eight dogs. If peak vest pressure was limited to 280 mm Hg, however, severe trauma was no longer observed. A study of the hemodynamics during and survival from prolonged resuscitation was then performed on three groups of seven dogs. Vest CPR was compared with manual CPR with either conventional (300 newtons) or high (430 newtons) sternal force. After induction of ventricular fibrillation, each technique was performed for 26 min. Defibrillation was then performed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vest inflation without simultaneous ventilation during cardiac arrest in dogs: improved survival from prolonged cardiopulmonary resuscitation. 377 22

A study was done comparing resuscitability and 24-hour neurologic outcome in fibrillating dogs that were treated with either phenylephrine (a primary alpha agonist) or epinephrine. Ventricular fibrillation was induced electrically in 18 dogs. After three minutes, standard CPR was instituted using a mechanical resuscitator. Dogs were given phenylephrine or epinephrine at nine minutes and defibrillation was attempted at 12 minutes. Dogs underwent hemodynamic monitoring and pharmacologic support, if necessary, for an additional 90 minutes. At four, eight, 12, and 24 hours, a standard neurologic examination was performed and deficit scores were assigned by an observer blinded to the drug given. Fourteen of the 18 dogs were resuscitated. There were no statistically significant differences in the epinephrine- or phenylephrine-treated groups with regard to number of animals resuscitated, time and interventions required for resuscitation, initial cardiac rhythm post resuscitation, or occurrence of ventricular fibrillation during resuscitation. No differences were found in arterial, central venous, or myocardial perfusion pressures during CPR. Phenylephrine-treated dogs tended to have higher mean pressures in the critical care period (15 to 30 minutes), although this was not significant. Total neurologic deficit scores were 127.8 +/- 83.8 for the phenylephrine-treated group and 129.4 +/- 87.4 for the epinephrine group. No significant differences were found in the level of consciousness, cranial nerve function, motor skills, or general behavior scores. We conclude that there is no difference in neurologic or cardiovascular outcome when phenylephrine is compared to epinephrine in a canine model of cardiac arrest and cardiopulmonary resuscitation.
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PMID:Comparison of epinephrine and phenylephrine for resuscitation and neurologic outcome of cardiac arrest in dogs. 380 61


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