Prolonged Cardiac Arrest In Dogs Research Articles

Rapidly induced hypothermia with extracorporeal lung and heart assist (ECLHA) improves the neurological outcome after prolonged cardiac arrest in dogs

We reported previously that therapeutic hypothermia with extracorporeal lung and heart assist (ECLHA) improved neurological outcome after 15 min cardiac arrest (CA) in dogs, although 45 min was needed to achieve hypothermia. We now investigate whether rapidly induced hypothermia with ECLHA (RHE) would result in a better outcome than slowly induced hypothermia with ECLHA (SHE) in dogs. Fifteen mongrel female dogs were divided into two groups: an RHE (n = 7) and an SHE (n = 8) group. Normothermic ventricular fibrillation was induced for 15 min and the animals were resuscitated by ECLHA. Rapid hypothermia was induced with a heat exchanger added to the ECLHA circuit in the RHE group, and by immersing the drainage tube of the ECLHA circuit in an ice water bath in the SHE group. Hypothermia (33 degrees C) was maintained for 20 h. The dogs were weaned from ECLHA at 24 h after resuscitation and treated for 96 h; neurological deficit scores (NDS) were measured throughout this period. It took 1.6+/-0.8 min to reach 33 degrees C in the RHE group and 49.5+/-12.1 min to reach 33 degrees C in the SHE group. There was no difference in survival rate between the two groups. The NDS at 96 h in the RHE group was better than that in the SHE group (26% (range: 10-28%) versus 32% (26-37%); p < 0.05) although there was no significant difference in NDS between the two groups until 72 h. Rapid hypothermic induction might be an important factor to improve neurological outcomes in prolonged CA models.

A moderate dose of propofol and rapidly induced mild hypothermia with extracorporeal lung and heart assist (ECLHA) improve the neurological outcome after prolonged cardiac arrest in dogs

Propofol has been shown to protect against neuronal damage induced by brain ischaemia in small animal models. We reported previously that mild hypothermia (33 degrees C) in combination with extracorporeal lung and heart assist (ECLHA) improved the neurological outcome in dogs with cardiac arrest (CA) of 15 min induced during normothermia. In the present study, we investigated the neuroprotective effect of propofol infusion under mild hypothermia with ECLHA in this model. Twenty-one female dogs (15 mongrel dogs and 6 beagles) were divided into three groups: Midazolam 0.1 mg/(kg h) infusion group (M, n=7), Propofol 2 mg/(kg h) infusion group (P2, n=7), Propofol 4 mg/(kg h) infusion group (P4, n=7). Normothermic ventricular fibrillation (VF) was induced in all dogs for 15 min, followed by brief ECLHA and 168 h of intensive care. The drug infusion was initiated at a constant rate after the restoration of spontaneous circulation (ROSC) to 24 h. Mild hypothermia (33 degrees C) was maintained for 20 h. Neurological deficit scores (NDS: 0%=normal, 100%=brain death) were evaluated for neurological function from 33 to 168 h. One dog in the M group died, and the remaining dogs survived for 168 h. The P4 group showed better neurological recovery compared with the M group (48 h, 21+/-16% versus 32+/-15%; 72 h, 7+/-6% versus 25+/-11%; 96 h, 6+/-6% versus 21+/-6%; 120 h, 5+/-5% versus 20+/-6%; 144 h, 4+/-4% versus 20+/-6%; 168 h, 4+/-4% versus 20+/-6%, p<0.05). One dog in the P2 and three dogs in the P4 group achieved full neurological recovery (NDS: 0%). The number of intact pyramidal cells in the hippocampal CA1 was greater in the propofol groups than midazolam group (p<0.05). The combination of propofol infusion at a rate of 4 mg/(kg h), 24h and rapidly induced mild hypothermia (33 degrees C) with ECLHA might provide a successful means of cerebral resuscitation from CA.

Part 7.4: Monitoring and Medications

This section provides an overview of monitoring techniques and medications that may be useful during CPR and in the immediate prearrest and postarrest settings. ### Assessment During CPR At present there are no reliable clinical criteria that clinicians can use to assess the efficacy of CPR. Although end-tidal CO2 serves as an indicator of cardiac output produced by chest compressions and may indicate return of spontaneous circulation (ROSC),1,2 there is little other technology available to provide real-time feedback on the effectiveness of CPR. ### Assessment of Hemodynamics #### Coronary Perfusion Pressure Coronary perfusion pressure (CPP = aortic relaxation [diastolic] pressure minus right atrial relaxation phase blood pressure) during CPR correlates with both myocardial blood flow and ROSC (LOE 3).3,4 A CPP of ≥15 mm Hg is predictive of ROSC. Increased CPP correlates with improved 24-hour survival rates in animal studies (LOE 6)5 and is associated with improved myocardial blood flow and ROSC in animal studies of epinephrine, vasopressin, and angiotensin II (LOE 6).5–7 When intra-arterial monitoring is in place during the resuscitative effort (eg, in an intensive care setting), the clinician should try to maximize arterial diastolic pressures to achieve an optimal CPP. Assuming a right atrial diastolic pressure of 10 mm Hg means that the aortic diastolic pressure should ideally be at least 30 mm Hg to maintain a CPP of ≥20 mm Hg during CPR. Unfortunately such monitoring is rarely available outside the intensive care environment. #### Pulses Clinicians frequently try to palpate arterial pulses during chest compressions to assess the effectiveness of compressions. No studies have shown the validity or clinical utility of checking pulses during ongoing CPR. Because there are no valves in the inferior vena cava, retrograde blood flow into the venous system may produce femoral vein pulsations.8 Thus palpation of a pulse in the femoral triangle may indicate venous rather than arterial …

Antioxidant Tempol enhances hypothermic cerebral preservation during prolonged cardiac arrest in dogs.

The authors are systematically exploring pharmacologic preservation for temporarily unresuscitable exsanguination cardiac arrest in dogs. They hypothesized that the antioxidant Tempol improves cerebral outcome when added to aortic saline flush at the start of cardiac arrest. In study A, no drug (n = 8), Tempol 150 mg/kg (n = 4), or Tempol 300 mg/kg (n = 4) was added to 25 mL/kg saline flush at 24 degrees C (achieving mild cerebral hypothermia) at the start of 20-minute cardiac arrest. In study B, no drug (n = 8) or Tempol 300 mg/kg (n = 7) was added to 50 mL/kg saline flush at 2 degrees C (achieving moderate cerebral hypothermia) at the start of 40-minute cardiac arrest. Cardiac arrest was reversed with cardiopulmonary bypass. Mild hypothermia lasted for 12 hours, controlled ventilation was sustained to 24 hours, and intensive care was provided for up to 72 hours. In study A, overall performance category 1 or 2 (good outcome) was achieved in all eight dogs treated with Tempol compared with three of eight dogs in the control group ( P = 0.03). In study B, good outcome was achieved in all seven dogs treated with Tempol versus only two of 8 dogs in the control group ( P = 0.007). In both studies, neurologic deficit scores were significantly better in the Tempol group, but not total histologic damage scores. At 72 hours, electron paramagnetic resonance spectroscopy of Tempol revealed direct evidence for its presence in the brain. Single- and double-strand DNA damage, nitrotyrosine immunostaining, total antioxidant reserve, and ascorbate acid levels were similar between groups, and thiol levels were decreased after Tempol in study B. The authors conclude that when added to aortic saline flush at the start of prolonged cardiac arrest, the antioxidant Tempol can enhance mild or moderate hypothermic cerebral preservation in terms of improved functional outcome. The mechanisms involved in this beneficial effect need further clarification.

Sodium bicarbonate improves the chance of resuscitation after 10 minutes of cardiac arrest in dogs

The likelihood of successful defibrillation and resuscitation decreases as the duration of cardiac arrest increases. Prolonged cardiac arrest is also associated with the development of acidosis. These experiments were designed to determine whether administration of sodium bicarbonate and/or adrenaline in combination with a brief period of cardiopulmonary resuscitation (CPR) prior to defibrillation would improve the outcome of prolonged cardiac arrest in dogs. Ventricular fibrillation (VF) was induced by a.c. shock in anaesthetised dogs. After 10 min of VF, animals received either immediate defibrillation (followed by treatment with bicarbonate or control) or immediate treatment with bicarbonate or saline (followed by defibrillation). Treatment with bicarbonate was associated with increased rates of restoration of spontaneous circulation. This was achieved with fewer shocks and in a shorter time. Coronary perfusion pressure was significantly higher in NaHCO 3-treated animals than in control animals. There were smaller decreases in venous pH in NaHCO 3-treated animals than in controls. The best outcome in this study was achieved when defibrillation was delayed for approximately 2 min, during which time NaHCO 3 and adrenaline were administered with CPR. The results of the present study indicate that in prolonged arrests bicarbonate therapy and a period of perfusion prior to defibrillation may increase survival.

Long-term mild hypothermia with extracorporeal lung and heart assist improves survival from prolonged cardiac arrest in dogs

Background and purpose: although normothermic extracorporeal lung and heart assist (ECLHA) improves cardiac outcomes, patients can not benefit from hypothermia-mediated brain protection. The present study evaluated the effects of long-term ECLHA with mild to moderate hypothermia (33°C) in a canine model of prolonged cardiac arrest. Methods: 15 dogs were assigned to either the hypothermic (seven dogs, 33°C) or normothermic group (eight dogs, 37.5°C). All dogs were induced to normothermic ventricular fibrillation (VF) for 15 min, followed by 24 h of ECLHA and 72 h of intensive care. The hypothermia group maintained core (pulmonary artery) temperature at 33°C for 20 h starting from resuscitation, then were rewarmed by 28 h. Outcome evaluations included: (1) mortality; (2) catecholamine dose; (3) time to extubation; (4) necrotic myocardial mass (g); and (5) neurological deficits score (NDS). Results: in the normothermic group five dogs died of cardiogenic shock and one dog succumbed to poor oxygenation. The two surviving dogs remained comatose (NDS 60.5±4.9%) with necrotic myocardial mass of 14.5±3.5 g. In the hypothermic group, one dog died from pulmonary dysfunction, the other six dogs survived. The surviving dogs showed brain damage (29.8±2.5%), but there was evidence of some brain-protective effect. The mass of necrotic myocardium was 4.2±1.3 g in the hypothermic group or 3.4 times smaller than in the normothermic group. The survival rate was significantly higher in the hypothermic than in the normothermic group ( P<0.05). The catecholamine requirement was also lower in the hypothermic than in the normothermic dogs ( P<0.05). Conclusions: Long-term mild to moderate hypothermia with ECLHA induced immediately after cardiac arrest improved survival as well as cerebral and cardiac outcomes.

Part 8: Advanced Challenges in Resuscitation

Part 8: Advanced Challenges in Resuscitation

Thiopental combination treatments for cerebral resuscitation after prolonged cardiac arrest in dogs. Exploratory outcome study

We postulate that mitigating the multifactorial pathogenesis of postischemic encephalopathy requires multifaceted treatments. In preparation for expensive definitive studies, we are reporting here the results of small exploratory series, compared with historic controls with the same model. We hypothesized that the brain damage mitigating effect of mild hypothermia after cardiac arrest can be enhanced with thiopental loading, and even more so with the further addition of phenytoin and methylprednisolone. Twenty-four dogs (four groups of six dogs each) received VF 12.5 min no-flow, reversed with brief cardiopulmonary bypass (CPB), controlled ventilation to 20 h, and intensive care to 96 h. Group 1 with normothermia throughout and randomized group 2 with mild hypothermia (from reperfusion to 2 h) were controls. Then, group 3 received in addition, thiopental 90 mg/kg i.v. over the first 6 h. Then, group 4 received, in addition to group 2 treatment, thiopental 30 mg/kg i.v. over the first 90 min (because the larger dose had produced cardiopulmonary complications), plus phenytoin 15 mg/kg i.v. at 15 min after reperfusion, and methylprednisolone 130 mg/kg i.v. over 20 h. All dogs survived. Best overall performance categories (OPC) achieved (OPC 1=normal, OPC 5=brain death) were better in group 2 than group 1 (<0.05) and numerically better in groups 3 or 4 than in groups 1 or 2. Good cerebral outcome (OPC 1 or 2) was achieved by all six dogs only in group 4 ( P<0.05 group 4 vs. 2). Best NDS were 44±3% in group 1; 20±14% in group 2 ( P=0.002); 21±15% in group 3 (NS vs. group 2); and 7±8% in group 4 ( P=0.08 vs. group 2). Total brain histologic damage scores (HDS) at 96 h were 156±38 in group 1; 81±12 in group 2 ( P<0.001 vs. group 1); 53±25 in group 3 ( P=0.02 vs. group 2); and 48±5 in group 4 ( P=0.02 vs. group 2). We conclude that after prolonged cardiac arrest, the already established brain damage mitigating effect of mild immediate postarrest hypothermia might be enhanced by thiopental, and perhaps then further enhanced by adding phenytoin and methylprednisolone.

Cerebral and systemic arteriovenous oxygen monitoring after cardiac arrest. Inadequate cerebral oxygen delivery

Background: After prolonged cardiac arrest, under controlled normotension, cardiac output and cerebral blood flow are reduced for several hours. This dog study documents for the first time the postarrest reduction in oxygen (O 2) delivery in relation to O 2 uptake for brain and entire organism. Methods: In eight dogs we used our model of ventricular fibrillation (VF) cardiac arrest of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled normotension, normoxemia, and mild hypocapnia to 24 h. Results: Between 4 and 24 h after cardiac arrest, cardiac output decreased by about 25% and the systemic arteriovenous Oz content difference doubled, while the calculated systemic O 2 utilization coefficient (O 2 UC) increased and the systemic venous PO 2 decreased, both not to critical levels. The cerebral arteriovenous O 2 content difference however, which was 5.6 ± 1.7 ml/dl before arrest, increased between 1 and 18 h, to 10.8 ± 3.2 ml/dl at 4 h. The cerebral O 2 UC increased and the cerebral venous Poz decreased, both to critical levels. Conclusions: After prolonged cardiac arrest in dogs with previously fit hearts, the reduction of O 2 transport to the brain is worse than its reduction to the whole organism. Monitoring these values might help in titrating life-support therapies.

Multifocal cerebral blood flow by Xe-CT and global cerebral metabolism after prolonged cardiac arrest in dogs. Reperfusion with open-chest CPR or cardiopulmonary bypass.

Using the stable xenon-enhanced computed tomography (Xe-CT) method in dogs, we studied local, regional and global cerebral blood flow (LCBF, rCBF and gCBF) in two sham experiments and nine cardiac arrest experiments. Within the same experiments without arrest, gCBF and rCBF values were reproducible and stable. LCBF values varied over time. In group I (n = 4), ventricular fibrillation cardiac arrest (no blood flow) of 10 min was reversed by open-chest cardiopulmonary resuscitation (CPR). In group II (n = 5), ventricular fibrillation cardiac arrest of 12.5 min was reversed by brief closed-chest cardiopulmonary bypass. This was followed by controlled ventilation, normotension, normoxia, normocarbia and normothermia to 4 h (n = 7) or 20 h (n = 2) postarrest. The postarrest CBF patterns were similar in both groups. Open-chest CPR during ventricular fibrillation generated near-baseline gCBF and lower LCBF ranges. During postarrest spontaneous circulation, transient diffuse hyperemia was without low-flow regions, longer in brain stem and basal ganglia than in neocortex. During delayed hypoperfusion at 1-4 h postarrest (n = 9), mean gCBF was 44-60% baseline, rCBF in primarily gray matter regions was 15-49 ml/100 cm3 per min and LCBF voxels with trickle-flow and low-flow values, in percent of CT cut area, were increased over baseline. Global CMRO2 (n = 3 of group II) recovered to near baseline values between 1 and 4 h postarrest, while gCBF and O2 delivery were about 50% baseline (mismatching of O2 uptake and O2 delivery).

Dynamic heterogeneity of cerebral hypoperfusion after prolonged cardiac arrest in dogs measured by the stable xenon/CT technique: a preliminary study.

After prolonged cardiac arrest and reperfusion, global cerebral blood flow (gCBF) is decreased to about 50% normal for many hours. Measurement of gCBF does not reveal regional variation of flow or permit testing of hypotheses involving multifocal no-flow or low-flow areas. We employed the noninvasive stable Xenon-enhanced Computerized Tomography (Xe/CT) local CBF (LCBF) method for use in dogs before and after ventricular fibrillation (VF) cardiac arrest of 10 min. This was followed by external cardiopulmonary resuscitation (CPR) and control of cardiovascular pulmonary variables to 7 h postarrest. In a sham (no arrest) experiment, the three CT levels studied showed normal regional heterogeneity of LCBF values, all between 10 and 75 ml/100 cm3 per min for white matter and 20 and 130 ml/100 cm3 per min for gray matter. In four preliminary CPR experiments, the expected global hyperemia at 15 min after arrest, was followed by hypoperfusion with gCBF reduced to about 50% control and increased heterogeneity of LCBF. Trickle flow areas (LCBF less than 10 ml/100 cm3 per min) not present prearrest, were interspersed among regions of low, normal, or even high flow. Regions of 125-500 mm3 with trickle flow or higher flows, in different areas at different times, involving deep and superficial structures migrated and persisted to 6 h, with gCBF remaining low. These preliminary results suggest: no initial no-reflow foci (less than 10 ml/100 cm3 per min) larger than 125 mm3 persisting through the initial global hyperemic phase; delayed multifocal hypoperfusion more severe than suggested by gCBF measurements; and trickle flow areas caused by dynamic factors.

External cardiopulmonary resuscitation preserves brain viability after prolonged cardiac arrest in dogs

Standard external cardiopulmonary resuscitation (CPR) steps A-B-C produce a low blood flow that may or may not preserve brain viability during prolonged cardiac arrest. A dog model was used with ventricular fibrillation (VF) of 20 minutes, reperfusion with brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 96 hours. A retrospective comparison was made of the results of one series, now called “group I” (n = 10)—which received CPR basic life support interposed from VF 10 to 15 minutes, and CPR advanced life support with epinephrine (without defibrillation) from VF 15 to 20 minutes—to the results of another series, now “control group II” (n = 10)—which received VF no flow (no CPR) for 20 minutes. All 20 dogs within protocol were resuscitated. All 10 of group I and 7 of group II survived to 96 hours. Pupillary light reflex returned after the start of cardiopulmonary bypass at 7.7 ± 3.7 minutes in CPR group I, versus 16.3 ± 7.4 minutes in control group II ( P = .032). At 96 hours postarrest, final overall performance categories (1, normal; 5, brain death) were better in group I. Six of 10 dogs achieved normality (overall performance category 1) in group I, as compared with none of 10 in group II ( P = .004). Final neurologic doficit score (0%, best; 100% worst) was lower (better) in group I (15% ± 20%) than in group II (51% ± 6%; P < .001). Final canine coma score (15, best; 3, worst) was higher (better) in group I (13.0 ± 2.8) than in group II (8.0 ± 1.3; P = .002). It was concluded that optimal standard external CPR steps A-B-C can sustain cerebral viability during prolonged VF cardiac arrest, even after no flow of 10 minutes.

Mild hypothermia cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs

This study was designed to explore the effect of mild cerebral and systemic hypothermia (34 degrees C) on outcome after prolonged cardiac arrest in dogs. After ventricular fibrillation with no flow of 10 min, and standard external CPR with epinephrine (low flow) from ventricular fibrillation time of 10 to 15 min, defibrillation and restoration of spontaneous normotension were between ventricular fibrillation time of 16 and 20 min. This procedure was followed by controlled ventilation to 20 hr postarrest and intensive care to 72 hr postarrest. In control group 1 (n = 10), core temperature was 37.5 degrees C; in control group 2 (n = 10), cooling was started immediately after restoration of spontaneous normotension; and in group 3 (n = 10), cooling was initiated with start of CPR. Cooling was by clinically feasible methods. Best overall performance categories achieved (1 = normal; 5 = brain death) were better in group 2 (p = .012) and group 3 (p = .005) than in group 1. Best neurologic deficit scores were 36 +/- 14% in group 1, 22 +/- 15% in group 2 (p = .02), and 19 +/- 18% in group 3 (p = .01). Brain histopathologic damage scores were also lower (better) in groups 2 (p = .05) and 3 (p = .03). Myocardial damage was the same in all three groups. Mild cerebral hypothermia started during or immediately after external CPR improves neurologic recovery.

Effect of Excitatory Amino Acid Receptor Blocker MK-801 on Overall, Neurologic, and Morphologic Outcome after Prolonged Cardiac Arrest in Dogs

Excitatory amino acids accumulating in the brain during ischemia may cause selective neuronal damage postischemia. This hypothesis was tested in a series of studies using MK-801, an N-methyl-D-aspartate (NMDA) receptor blocker, in a reproducible outcome model of prolonged cardiac arrest in dogs. After normothermic ventricular fibrillation cardiac arrest, the dogs were resuscitated with closed-chest femoral veno-arterial cardiopulmonary bypass. At 4 h they were separated from bypass, ventilation was controlled for 20 h, and intensive care was continued to 96 h. In Study I, ventricular fibrilation cardiac arrest (no-flow) was 17 min; starting immediately with reperfusion, MK-801 1200 mg/kg (n = 5) or an equal volume of placebo (n = 5) was infused over 12 h in blinded, randomized fashion. In Study II, the duration of the no-flow period was reduced to 15 min, and MK-801 2400 mg.kg-1 (n = 4) or placebo (n = 4) was infused. In Study III, no-flow lasted for 15 min, and MK-801 2400 mg/kg was started 30 min before ventricular fibrillation (n = 4); comparison was with Study II controls. In all three studies, MK-801 plasma concentrations peaked at greater than 50 ng/ml and were 15-30 ng/ml over 12 h. All 22 dogs of experiments within protocol survived with severe brain damage. MK-801 delayed return of pupillary reactivity, EEG activity, consciousness, and respiration, necessitating longer periods of controlled ventilation. Neurologic deficit scores, overall performance categories, and brain and heart morphologic damage scores at 96 h did not differ between placebo and MK-801 pretreatment or post-treatment groups. These negative outcome results after prolonged cardiac arrest do not negate the hyperexcitability hypothesis of selective vulnerability, but suggest the existance of additional mechanisms of secondary brain damage.

Myocardial perfusion pressure: a predictor of 24-hour survival during prolonged cardiac arrest in dogs.

Myocardial perfusion pressure, defined as the aortic diastolic pressure minus the right atrial diastolic pressure, correlates with coronary blood flow during cardiopulmonary resuscitation (CPR) and predicts initial resuscitation success. Whether this hemodynamic parameter can predict 24-h survival is not known. We examined the relationship between myocardial perfusion pressure and 24-h survival in 60 dogs that underwent prolonged (20 min) ventricular fibrillation and CPR. Forty-two (70%) animals were initially resuscitated and 20 (33%) survived for 24 h. Myocardial perfusion pressure was significantly greater when measured at 5, 10, 15 and 20 min of ventricular fibrillation in the resuscitated animals than in the non-resuscitated animals (P less than 0.01). Likewise, the myocardial perfusion pressure was also greater in the animals that survived 24 h than in animals that were resuscitated, but died before 24 h (P less than 0.02). Myocardial perfusion pressure measured after 10 min of CPR was 11 +/- 2 mmHg in animals never resuscitated, 20 +/- 3 mmHg in those resuscitated that died before 24 h and 29 +/- 2 mmHg in those that survived 24 h (P less than 0.05). A myocardial perfusion pressure at 10 min of CPR of 20 mmHg or less is an excellent predictor of poor survival (negative predictive value = 96%). Myocardial perfusion pressure is a useful index of CPR effectiveness and therefore may be a useful guide in helping to optimize resuscitation efforts.

Cardiopulmonary bypass after prolonged cardiac arrest in dogs

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)

Cardiopulmonary bypass for resuscitation after prolonged cardiac arrest in dogs

Cardiopulmonary bypass for resuscitation after prolonged cardiac arrest in dogs