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PubMed2006

Small-volume fluid resuscitation with hypertonic saline prevents inflammation but not mortality in a rat model of hemorrhagic shock.

Hemorrhage remains a primary cause of death in civilian and military trauma. Permissive hypotensive resuscitation is a possible approach to reduce bleeding in patients until they can be stabilized in an appropriate hospital setting. Small-volume resuscitation with hypertonic saline (HS) is of particular interest because it allows one to modulate the inflammatory response to hemorrhage and trauma. Here, we tested the utility of permissive hypotensive resuscitation with hypertonic fluids in a rat model of hemorrhagic shock. Animals were subjected to massive hemorrhage [mean arterial pressure (MAP) = 30 - 35 mmHg for 2 h until decompensation] and partially resuscitated with a bolus dose of 4 mL/kg of 7.5% NaCl (HS), hypertonic hydroxyl ethyl starch (HHES; hydroxyl ethyl starch + 7.5% NaCl), or normal saline (NS) followed by additional infusion of Ringer solution to maintain MAP at 40 to 45 mmHg for 40 min (hypotensive state). Finally, animals were fully resuscitated with Ringer solution and the heparinized shed blood. Hypotensive resuscitation with NS caused a significant increase in plasma interleukin (IL)-1beta, IL-6, IL-2, interferon gamma (IFNgamma), IL-10, and granulocyte-macrophage colony stimulating factor (GM-CSF). This increase was blocked by treatment with HS. HHES treatment significantly reduced the increase of IL-1beta and IL-2 but not that of the other cytokines studied. Despite the strong effects of HS and HHES on cytokine production, both treatments had little effect on plasma lactate, base excess (BE), white blood cell (WBC) count, myeloperoxidase (MPO) content, and the wet/dry weight ratio of the lungs. Moreover, on day 7 after shock, the survival rate in rats treated with HS was markedly, but not significantly, lower than that of NS-treated animals (47% vs. 63%, respectively). In summary, hypotensive resuscitation with hypertonic fluids reduces the inflammatory response but not lung tissue damage or mortality after severe hemorrhagic shock.

Animals↗
PubMed2006

Synergistic effects of recombinant human soluble thrombomodulin and fluid-volume resuscitation in a rat lethal crush injury model.

Severe crush injury results in a high mortality rate because of acute circulatory failure and hyperkalemia. The purpose of this study was to evaluate whether administration of prophylactic-recombinant human soluble thrombomodulin (rhsTM) and/or fluid-volume resuscitation before reperfusion attenuates severe crush injury in rats. Both hindlimbs of anesthetized rats were compressed for 6 h under blocks weighing 3.5 kg each, followed by 3 h of reperfusion. In the first group, fluid resuscitation with normal saline (1 mL/kg/h) was performed throughout the experiment. In the second group, volume resuscitation treatment with normal saline (10 mL/kg/h) was initiated 60 min before the end of the crush period and was continued until the end of the experiment. In the third group, normal saline-resuscitation treatment plus rhsTM (3 mg/kg) was performed. In the fourth group, volume resuscitation treatment plus rhsTM was performed. Blood samples were collected 6 h after the end of the crush period. Complete blood count and platelets were measured. In addition, serum lactate, base deficit, serum potassium, creatine phosphokinase, blood urea nitrogen, creatinine, myoglobin, and some cytokines were evaluated. In another experiment, survival of each group was monitored for 72 h after the end of the crush period. Combined administration of rhsTM and volume resuscitation significantly decreased hemoconcentration and hyperkalemia. The serum interleukin-6 level and mortality were also significantly improved in the combination group compared with those in the other groups. We conclude that prophylactic combination of rhsTM administration and volume resuscitation may be an effective therapy for severe crush injury.

Animals↗
PubMed2004

Resuscitation with 100% oxygen causes intestinal glutathione oxidation and reoxygenation injury in asphyxiated newborn piglets.

OBJECTIVE: To compare mesenteric blood flow, oxidative stress, and mucosal injury in piglet small intestine during hypoxemia and reoxygenation with 21%, 50%, or 100% oxygen. SUMMARY BACKGROUND DATA: Necrotizing enterocolitis is a disease whose pathogenesis likely involves hypoxia-reoxygenation and the generation of oxygen-free radicals, which are known to cause intestinal injury. Resuscitation of asphyxiated newborns with 100% oxygen has been shown to increase oxidative stress, as measured by the glutathione redox ratio, and thus may predispose to free radical-mediated tissue injury. METHODS: Newborn piglets subjected to severe hypoxemia for 2 hours were resuscitated with 21%, 50%, or 100% oxygen while superior mesenteric artery (SMA) flow and hemodynamic parameters were continuously measured. Small intestinal tissue samples were analyzed for histologic injury and levels of oxidized and reduced glutathione. RESULTS: SMA blood flow decreased to 34% and mesenteric oxygen delivery decreased to 9% in hypoxemic piglets compared with sham-operated controls. With reoxygenation, SMA blood flow increased to 177%, 157%, and 145% of baseline values in piglets resuscitated with 21%, 50%, and 100% oxygen, respectively. Mesenteric oxygen delivery increased to more than 150% of baseline values in piglets resuscitated with 50% or 100% oxygen, and this correlated significantly with the degree of oxidative stress, as measured by the oxidized-to-reduced glutathione ratio. Two of eight piglets resuscitated with 100% oxygen developed gross and microscopic evidence of pneumatosis intestinalis and severe mucosal injury, while all other piglets were grossly normal. CONCLUSIONS: Resuscitation of hypoxemic newborn piglets with 100% oxygen is associated with an increase in oxygen delivery and oxidative stress, and may be associated with the development of small intestinal hypoxia-reoxygenation injury. Resuscitation of asphyxiated newborns with lower oxygen concentrations may help to decrease the risk of necrotizing enterocolitis.

Analysis of Variance↗
PubMed2003

Blood pressure at which rebleeding occurs after resuscitation in swine with aortic injury.

BACKGROUND: The appropriateness of vigorous fluid resuscitation to normal blood pressure following hemorrhage in uncontrolled bleeding has recently been questioned due to the possibility of dislodging clots and exacerbating hemorrhage. To develop a rational blood pressure target that maximizes the metabolic benefits of resuscitation without causing increased blood loss, it was first necessary to determine whether there is a reproducible mean arterial pressure (MAP) at which rebleeding occurs. The purpose of this study was to explore the relationship between the rate and time of resuscitation after injury and the rebleeding MAP in an uncontrolled hemorrhage model. METHODS: Sixty-two anesthetized pigs were instrumented with catheters and splenectomized, and suction tubes were placed in the lateral peritoneal recesses to continuously capture shed blood. With the abdomen open, an aortotomy was made in the infrarenal aorta. At either 5, 15, or 30 minutes after the end of the initial hemorrhage, resuscitation with warmed lactated Ringer's solution was begun at either 100 or 300 mL/min. The rebleeding MAP was determined at the moment blood appeared in the suction tubes. RESULTS: The average pressure at the rebleeding point for all animals was MAP = 64 +/- 2, Systolic = 94 +/- 3, and Diastolic = 45 +/- 2 mm Hg. The pressure at which rebleeding occurred in this aortotomy model was not affected by either time of resuscitation (5-30 min), nor was the rebleeding pressure affected by the rate (100 vs. 300 mL/min) of resuscitation. CONCLUSIONS: There was a reproducible pressure at which rebleeding occurred in this model of uncontrolled hemorrhage. The optimal endpoint of resuscitation in patients without definitive hemorrhage control would then be below this rebleeding pressure.

Animals↗
PubMed2004

Building a better fluid for emergency resuscitation of traumatic brain injury.

UNLABELLED: Hextend (HEX) is a colloid solution that is FDA-approved for volume expansion during surgery. ATL-146e is a novel adenosine A2A receptor agonist that has anti-inflammatory, neuroprotective, and coronary vasodilator properties. Three series of experiments were designed to evaluate the therapeutic potential of HEX+/-ATL-146e for emergency resuscitation from traumatic brain injury (TBI) + hemorrhagic hypotension. METHODS: In the first two studies in vivo, anesthetized, ventilated pigs (30-45 kg) received a fluid percussion TBI, 45% arterial hemorrhage, and 30 minutes shock period. In Series 1, resuscitation consisted of unlimited crystalloid (n = 8) or HEX (n = 8) to correct systolic arterial pressure >100 mm Hg and heart rate <100 bpm for the first 60 minutes ("emergency phase"), and then maintain cerebral perfusion pressure (CPP) > 70 mm Hg for 60-240 minutes. In Series 2 (n = 31), resuscitation consisted of a 1 L bolus of HEX + ATL-146e (10 ng/kg/min, n = 10) or HEX +placebo (n = 10) followed by crystalloid to the same endpoints. In Series 3 in vivo, the hemodynamic response evoked by 0, 10, 50, or 100 ng/kg/min ATL-146e was measured before or 60 minutes after HEX resuscitation from 45% hemorrhage. RESULTS: Following TBI+hemorrhage, there were 4/22 deaths in series 1 and 11/31 deaths in series 2. In those alive at 30 minutes, mean arterial pressure, cardiac index, mixed venous O2 saturation, and cerebral venous O2 saturation were all reduced by 40-60%, while heart rate and lactate were increased 2-5 fold. With no resuscitation (n = 2), there was minimal hemodynamic compensation and progressive acidosis. Upon resuscitation, these values corrected but intracranial pressure progressively rose from <5 mm Hg to 15-20 mm Hg. Series 1: With HEX (n = 8) versus crystalloid (n = 8), CPP was less labile, acid/base was maintained, and the fluid requirement was reduced by 60% (all p < 0.05) Series 2: With ATL-146e (n = 10) versus placebo (n = 10), stroke volume and cardiac output were improved by 40-60%, and the fluid requirement was reduced by 30% (all p < 0.05). Series 3: ATL-146e caused a dose-related increase (p < 0.05) in stroke volume after, but not before, hemorrhage. The effects on pre-load, afterload, and heart rate were similar before and after hemorrhage. CONCLUSIONS: HEX alone is a safe and efficacious low volume alternative to initial crystalloid resuscitation after TBI. An adenosine A2A agonist combined with 1 L of HEX safely and effectively counteracted a decrease in cardiac performance noted after TBI+hemorrhage without causing hypotension or bradycardia.

Animals↗
PubMedDate not supplied

Neonatal resuscitation educational experience of staff in New South Wales and Australian Capital Territory hospitals.

OBJECTIVE: There is international recognition that health personnel involved in deliveries should be adequately trained in neonatal resuscitation. A survey was carried out in New South Wales (NSW) and the Australian Capital Territory (ACT) to ascertain the type, frequency and availability of training in neonatal resuscitation to staff who may need to resuscitate an infant at birth. The survey included a self-perception rating of confidence and competence in neonatal resuscitation. METHODS: Questionnaires were sent to 117 hospitals carrying out deliveries in NSW and ACT. Questionnaires were distributed to staff members who may be present at a delivery in a designated 24-h period. RESULTS: In total, 1457 questionnaires from 101 hospitals were returned and analysed. Overall response rate was 86.3% with 96.1% able to be assigned to tertiary, urban non-tertiary or rural areas. Eighty-five per cent of tertiary respondents had a training programme available to them compared with 59% of urban non-tertiary staff and 31% of rural practitioners. Approximately one-third of respondents in rural and urban non-tertiary units had either never been trained or had training more than 2 years before the survey. In rural areas more than 25% staff were not confident in their resuscitation skills and only 9% felt very competent. CONCLUSION: Three-quarters of all births in NSW and ACT take place in rural or urban non-tertiary hospitals where one-third of health personnel are inadequately trained in neonatal resuscitation and many do not feel confident in their skills. Effective neonatal resuscitation training for these areas is urgently required.

Australian Capital Territory↗
PubMed1992

Outcomes of skilled cardiopulmonary resuscitation in a long-term-care facility: futile therapy?

OBJECTIVE: To assess whether cardiopulmonary resuscitation performed by in-house physicians is effective for long-term-care residents. DESIGN: Retrospective chart review. SETTING: Long-term-care facility with an intermediate care unit, skilled care unit, and a convalescent and assessment unit at a retirement community for veterans. PARTICIPANTS: All residents resuscitated from April 1987 to August 1990. All participants were male. The mean age was 75 years +/- 7.3 (range 42-93 years). MAIN OUTCOME MEASUREMENTS: Charts were abstracted for demographics, advanced directives information, information about the arrest, and post-resuscitation course. RESULTS: Forty-five elderly residents underwent resuscitation during this period. Nine residents (20%) were successfully resuscitated, with seven dying within 24 hours of hospitalization. No residents survived to return to long-term care (95% CI, 0-7%). The diagnoses were consistent with age-related chronic disease. Seventeen (38%) arrests were witnessed. The predominant rhythm at onset of resuscitation was asystole. CONCLUSION: We conclude that cardiopulmonary resuscitation, even when performed by a trained and experienced physician and team, has limited benefit for elderly long-term-care populations.

Adult↗
PubMed1995

Multiple resuscitation regimens in a near-fatal porcine aortic injury hemorrhage model.

OBJECTIVE: To compare early and delayed blood administrations in animals subjected to near-fatal hemorrhage in the presence of a vascular injury and resuscitated to different mean arterial pressures (MAPs). METHODS: Fifty-four immature swine with 4-mm infrarenal aortic tears were bled to a pulse pressure of 5 torr and then resuscitated (estimated blood loss 40 to 45 mL/kg). Groups I, II, and III were resuscitated with shed blood at a rate of 2 mL/kg/min, followed by normal saline at a rate of 6 mL/kg/min. Groups IV, V, and VI received the same fluids in reverse order. The fluids were infused intermittently to maintain MAPs of 40, 60, and 80 torr. The animals were observed for 60 minutes or until death. RESULTS: The animals resuscitated to a MAP of 80 torr experienced significantly higher intraperitoneal hemorrhage volumes and mortality than did the animals intentionally maintained hypotensive, regardless of whether blood or normal saline was administered first. There was no significant difference in mortality or hemorrhage volumes between any of the groups intentionally maintained hypotensive. The animals maintained at a MAP of 60 torr were significantly less acidotic than were the animals resuscitated with the same fluid regimen but to a MAP of 40 torr. Early blood administration also minimized the acidosis associated with hypotensive resuscitation. CONCLUSION: In this model of near-fatal hemorrhage with a vascular injury, maintenance of the hypotensive state produced comparable improvements in one-hour survival and reductions in hemorrhage volume regardless of whether blood or saline was administered first. Although hypotensive resuscitation resulted in improved outcome, it was associated with significant acidosis. This effect was minimized with moderate rather than severe underresuscitation and early blood administration.

Analysis of Variance↗
PubMed1992

Survey of 3765 cardiopulmonary resuscitations in British hospitals (the BRESUS Study): methods and overall results.

OBJECTIVE: To determine the circumstances, incidence, and outcome of cardiopulmonary resuscitation in British hospitals. DESIGN: Hospitals registered all cardiopulmonary resuscitation attempts for 12 months or longer and followed survival to one year. SETTING: 12 metropolitan, provincial, teaching, and non-teaching hospitals across Britain. SUBJECTS: 3765 patients in whom a resuscitation attempt was performed, including 927 in whom the onset of arrest was outside the hospital. MAIN OUTCOME MEASURE: Survival after initial resuscitation, at 24 hours, at discharge from hospital, and at one year, calculated by the life table method. RESULTS: There were 417 known survivors at one year, with 214 lost to follow up. By life table analysis for every eight attempted resuscitations there were three immediate survivors, two at 24 hours, 1.5 leaving hospital alive, and one alive at one year. Survival at one year was 12.5% including out of hospital cases and 15.0% not including these cases. Each hospital year averaged 30 survivors at one year: three who had an arrest outside hospital, seven who had one in the accident and emergency department, seven in the cardiac care unit, 10 in the general wards, and three in other, non-ward areas. Within the hospitals survival rates were best in those who had an arrest in the accident and emergency department, the cardiac care unit, or other specialised units. Outcome varied 12-fold in subgroups defined by age, type of arrest, and place of arrest. CONCLUSION: 71% of the mortality at one year in patients undergoing attempted resuscitation occurred during the initial arrest. Hospital resuscitation is life saving and cost effective and warrants appropriate attention, training, coordination, and equipment.

Age Factors↗
PubMed2004

Prospective observational study on the incidence of medication errors during simulated resuscitation in a paediatric emergency department.

OBJECTIVES: To characterise the incidence and nature of medication errors during paediatric resuscitations. DESIGN: A prospective observational study of simulated emergencies. SETTING: Emergency department of a tertiary paediatric hospital. PARTICIPANTS: Teams that included a clinician who commonly leads "real" resuscitations, at least two assisting physicians, and two or three paediatric nurses. INTERVENTIONS: The teams conducted eight mock resuscitations, including ordering medications. Exercises were videotaped and drugs ordered and administered during the resuscitation were recorded. Syringes and drugs prepared during the resuscitation were collected and analysed for concentrations and actual amounts. MAIN OUTCOME MEASURES: Number and type of drug errors. RESULTS: Participants gave 125 orders for medications. In 21 (17%) of the orders the exact dose was not specified. Nine dosing errors occurred during the ordering phase. Of these errors, five were intercepted before the drug reached the patient. Four 10-fold errors were identified. In nine (16%) out of 58 syringes analysed, measured drug concentrations showed a deviation of at least 20% from the ordered dose. A large deviation (at least 50%) from the expected dose was found in four (7%) cases. CONCLUSIONS: Medication errors commonly occur during all stages of paediatric resuscitation. Many errors could be detected only by analysing syringe content, suggesting that such errors may be a major source of morbidity and mortality in resuscitated children.

Child↗
PubMed2001

Evaluation of the role of the neonatal nurse practitioner in resuscitation of preterm infants at birth.

BACKGROUND: Changes in the work patterns and numbers of medical staff in training grades pose a significant challenge to those responsible for the provision of an effective clinical neonatal service. Advanced neonatal nurse practitioners (ANNPs) may have a role in this changing neonatal service. The effectiveness of the ANNP has been established in North America but has not been properly evaluated in the United Kingdom. AIM: To evaluate the effectiveness of ANNPs in resuscitation of preterm babies at birth against the standard set by junior medical staff. SETTING: Regional neonatal intensive care unit. METHOD: Retrospective analysis of resuscitation details, other basic data, and clinical outcomes of 245 preterm (< 33 weeks gestation) babies born in Liverpool Women's Hospital between January 1998 and April 1999. RESULTS: Resuscitation teams led by ANNPs provided the same resuscitation interventions as those provided by medically led teams. Although babies resuscitated by ANNP led teams were no more likely to be intubated, they were intubated more quickly and received surfactant sooner (p = 0.0001) than babies resuscitated by medically led teams. Babies attended by ANNP led teams were less likely to be hypothermic on admission to the neonatal unit (p = 0.013). CONCLUSION: ANNPs are effective in the resuscitation of preterm babies at birth.

Clinical Competence↗
PubMed1993

Out-of-hospital resuscitation in East Sussex: 1981 to 1989.

OBJECTIVE: To assess the impact of extended training in advanced life support on the outcome of resuscitation. DESIGN: Analysis of the successful resuscitations from 1981 to 1989. SETTING: Brighton and East Sussex. RESULTS: 248 patients were resuscitated from cardiac or respiratory arrest in the community and subsequently survived to leave hospital. Their mean age was 64 years and one year survival was 77%. In most cases the cause of collapse was cardiac but 38 (15%) suffered a respiratory arrest. In 140 of the successful resuscitations (56%) collapse occurred before the arrival of the ambulance. Basic life support, with ventilation and chest compression where necessary, was sufficient to revive 35 (14%) of the patients. Defibrillation was also required in 107 patients (43%), and in a further 106 patients (43%) who had prolonged cardiorespiratory arrest requiring endotracheal intubation and the use of several drugs. Review of ambulance forms and case notes showed that in 87 cases (35%) the abilities of the paramedical ambulance staff in advanced resuscitation techniques contributed decisively to the success of resuscitation. These skills are illustrated by eight case reports. CONCLUSIONS: Extended training for ambulance staff increases the likelihood of successful resuscitation from out-of-hospital cardiopulmonary arrest. Though instruction in defibrillation must have the highest priority, full paramedical training can bring appreciable additional benefits.

Adolescent↗
PubMed1994

Effect of bystander initiated cardiopulmonary resuscitation on ventricular fibrillation and survival after witnessed cardiac arrest outside hospital.

OBJECTIVE: To describe the proportion of patients who were discharged from hospital after witnessed cardiac arrest outside hospital in relation to whether a bystander initiated cardiopulmonary resuscitation. PATIENTS: All patients with witnessed cardiac arrest outside hospital before arrival of the ambulance and in whom cardiopulmonary resuscitation was attempted by the emergency medical service in Gothenburg during 1980-92. RESULTS: Cardiopulmonary resuscitation was initiated by a bystander in 18% (303) of 1,660 cases. In this group 69% had ventricular fibrillation at first recording compared with 51% in the remaining patients (P < 0.001). Among patients in whom cardiopulmonary resuscitation had been initiated by a bystander 25% were discharged alive versus 8% of the remaining patients (P < 0.001). Independent predictors of survival were in order of significance: initial arrhythmia (P < 0.001), interval between collapse and arrival of first ambulance (P < 0.001), cardiopulmonary resuscitation initiated by a bystander (P < 0.001), and age (P < 0.01). Among patients who were admitted to hospital alive 30% of patients in whom cardiopulmonary resuscitation had been initiated by a bystander compared with 58% of remaining patients (P < 0.001) had brain damage and died in hospital. Corresponding figures for death in association with myocardial damage were 18% and 29% respectively (P < 0.01). CONCLUSIONS: Cardiopulmonary resuscitation initiated by a bystander maintains ventricular fibrillation and triples the chance of surviving a cardiac arrest outside hospital. Furthermore, it seems to protect against death in association with brain damage as well as with myocardial damage.

Age Factors↗
PubMed2000

Futility has no utility in resuscitation medicine.

"Futility" is a word which means the absence of benefit. It has been used to describe an absence of utility in resuscitation endeavours but it fails to do this. Futility does not consider the harms of resuscitation and we should consider the balance of benefit and harm that results from our resuscitation endeavours. If a resuscitation is futile then any harm that ensues will bring about an unfavourable benefit/harm balance. However, even if the endeavour is not futile, by any definition, the benefit/harm balance may still be unfavourable if the harms that ensue are great. It is unlikely that we will ever achieve a consensus definition of futility and certainly not one that is applicable to every patient undergoing resuscitation. In the meantime our use of the term "futile", in the mistaken belief that it tells us whether it is worth resuscitating or not, has no utility as it will never succeed in telling us this. Furthermore we risk causing offence by use of the term and we risk harming the patient's autonomy by using futility as an overriding force. Instead we should consider the utility of our endeavours, for which an assessment of the harms of resuscitation should be added to our considerations of its benefit. This balance of benefit and harm should then be evaluated as best it can be from the patient's perspective. The words futile and futility should be abandoned by resuscitationists.

Decision Making↗
PubMed1999

Changes in resistance vessels during hemorrhagic shock and resuscitation in conscious hamster model.

The unanesthetized hamster dorsal skinfold preparation was used to monitor diameters and blood flow rates in resistance arteries (small arteries, A0: diameter, 156 +/- 23 micrometers) and capacitance vessels (small veins, V0: 365 +/- 64 micrometers), during 45 min of hemorrhagic shock at 40 mmHg mean arterial pressure (MAP) and resuscitation. A0 and V0 vessels constricted significantly to 52 and 70% of the basal values, respectively, whereas precapillary arterioles (A1-A4, 8-60 micrometers) and collecting venules (VC-VL, 26-80 micrometers) did not change or tended to dilate. Blood flow rates in the microvessels declined to <20% of the basal values. Resuscitation with shed autologous blood (SAB) showed incomplete recovery of A0 and V0 diameters even 2 h after resuscitation (71 +/- 14% and 81 +/- 18%, respectively, of basal value), whereas other vessels did not change significantly. The behavior of A0 diameter coincided with the incomplete recovery of blood flow rates in all the vessels (ca. 50%) according to Poiseuille's law, and the incomplete recovery of functional capillary density (ca. 75%). Resuscitation with 8% human serum albumin in saline (HSA) tended to show higher levels of A0 constriction and A4 dilation and lowered blood flow rates. Resuscitation with SAB restored tissue PO2 27 +/- 10 mmHg after 2 h, which was near control levels (28 +/- 5 mmHg), whereas resuscitation with HSA caused tissue PO2 to remain significantly depressed (6 +/- 2 mmHg), and flow rates were significantly lower than resuscitation with SAB. These results indicate that response of the A0 vessels is the crucial determinant of blood flow in the observed area. The constriction of A0 may help sustain MAP, and constriction of V0 may enhance blood redistribution from the skin to the vital organs under the hypotensive condition.

Animals↗
PubMed1993

Regional blood flow during closed-chest cardiac resuscitation in rats.

Quantitative measurement of regional blood flow during cardiac arrest and resuscitation has been confined to large animals. We report on a rodent model utilizing radioactive microspheres during cardiac arrest and resuscitation for investigation of regional blood flow. Ventricular fibrillation was electrically induced in 10 pentobarbital-anesthetized Sprague-Dawley rats. Resuscitation was attempted by precordial compression followed by external direct current countershock. During precordial compression, cardiac output corresponded to 12% of prearrest flow. Similarly low flows were observed in the myocardium and brain. However, much lower flows were observed in the adrenal glands, kidneys, intra-abdominal viscera, skin, and skeletal muscle. Five of ten animals were successfully resuscitated. During precordial compression, resuscitated animals had significantly higher cardiac output (13.1 +/- 4.1 vs. 8.6 +/- 1.46 ml/min), myocardial blood flow (0.70 +/- 0.24 vs. 0.22 +/- 0.15 ml.min-1.g-1), cerebral blood flow (0.17 +/- 0.04 vs. 0.06 +/- 0.02 ml.min-1.g-1), and adrenal blood flow (1.09 +/- 0.60 vs. 0.27 +/- 0.16 ml.min-1.g-1). Thirty minutes after successful resuscitation, cardiac output and myocardial, cerebral, renal, and adrenal blood flows and blood flow to splanchnic viscera (with the exception of the spleen) had returned to > or = 70% of prearrest flows. These studies confirm the conclusion of earlier investigations in larger animals that visceral blood flow during cardiac arrest and precordial compression is preferentially distributed to the brain and myocardium. Successful cardiac resuscitation is contingent on threshold levels of myocardial blood flow that exceed 0.4 ml.min-1.g-1.

Adrenal Glands↗
PubMedDate not supplied

Diaspirin cross-linked hemoglobin fails to improve left ventricular diastolic function after fluid resuscitation from hemorrhagic shock.

In severe hemorrhagic shock, left ventricular (LV) diastolic dysfunction is an early sign of cardiac failure due to compromised myocardial oxygenation. Immediate fluid replacement or, in particular, administration of a hemoglobin-based oxygen carrier (diaspirin cross-linked hemoglobin; DCLHb) improves myocardial oxygenation; therefore, positive effects on LV diastolic function could be expected. The effects of fluid resuscitation from severe hemorrhagic shock with DCLHb were investigated in 20 anesthetized domestic pigs. After generation of a critical left anterior descending coronary artery stenosis (narrowing of the artery until disappearance of reactive hyperemia after a 10-second complete vessel occlusion), hemorrhagic shock (mean arterial blood pressure 45 mm Hg) was induced within 15 min by controlled blood withdrawal and maintained for 60 min. Fluid resuscitation consisted of replacement of the plasma volume withdrawn during hemorrhage by infusion of either 10% DCLHb (DCLHb group, n = 10) or 8% human serum albumin (HSA) oncotically matched to DCLHb (HSA group, n = 10). After completion of resuscitation, an observation period of 60 min elapsed. Measurements of central hemodynamics, myocardial oxygenation, and LV diastolic function were performed at baseline, after induction of critical coronary artery stenosis, after 60 min of hemorrhagic shock, immediately after resuscitation, and 60 min later. While 5 out of 10 animals treated with HSA died within the first 20 min after fluid resuscitation from acute LV pump failure, all DCLHb-treated animals survived until the end of the protocol (p < 0.05). Despite superior myocardial oxygenation due to augmentation of the arterial O(2) content as well as of coronary perfusion pressure, no beneficial effects on LV diastolic function were observed after infusion of DCLHb. Peak velocity of LV pressure decrease (dp/dt(min)) did not reveal significant differences between the two groups. Immediately after completion of fluid resuscitation with DCLHb, the time constant of LV diastolic relaxation (tau) was prolonged when compared with HSA-treated animals (p < 0.05), indicating retardation of early LV diastolic relaxation. Our data suggest that DCLHb fails to improve LV diastolic function after fluid resuscitation from severe hemorrhagic shock. However, positive effects on myocardial perfusion and oxygenation result in a significant reduction of the mortality of severe hemorrhagic shock.

Animals↗
PubMed2003

Sodium-hydrogen exchange inhibition during ventricular fibrillation: Beneficial effects on ischemic contracture, action potential duration, reperfusion arrhythmias, myocardial function, and resuscitability.

BACKGROUND: Inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) is emerging as a promising novel strategy for ameliorating myocardial injury associated with ischemia and reperfusion. We investigated whether NHE-1 inhibition (with cariporide) could minimize mechanical and electrical myocardial abnormalities that develop during ventricular fibrillation (VF) and improve outcome using a porcine model of closed-chest resuscitation. METHODS AND RESULTS: Two groups of 8 pigs each were subjected to 8 minutes of untreated VF and randomized to receive either a 3-mg/kg bolus of cariporide or 0.9% NaCl immediately before an 8-minute interval of conventional closed-chest resuscitation. Cariporide prevented progressive increases in left ventricular free-wall thickness (from 1.0+/-0.2 to 1.5+/-0.3 cm with NaCl, P<0.001 versus 0.9+/-0.1 to 1.1+/-0.3 cm with cariporide, P=NS), maintained the coronary perfusion pressure above resuscitability thresholds (10+/-8 versus 19+/-3 mm Hg before attempting defibrillation, P<0.05), and increased resuscitability (2 of 8 versus 8 of 8, P<0.005). In 2 additional groups of 4 pigs each subjected to a briefer interval of untreated VF, cariporide ameliorated postresuscitation shortening of the action potential duration (APD) at 30%, 60%, and 90% repolarization (ie, APD60 at 2 minutes after resuscitation; 75+/-29 versus 226+/-16 ms, P<0.05), minimized postresuscitation ventricular ectopic activity preventing recurrent VF, and lessened postresuscitation myocardial dysfunction. CONCLUSIONS: NHE-1 inhibition may represent a highly potent novel strategy for resuscitation from VF that can ameliorate myocardial manifestations of ischemic injury and improve the effectiveness and outcome of closed-chest resuscitation.

Action Potentials↗