Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospital setting

IntroductionThere has been increased interest in the use of capnometry in recent years. During cardiopulmonary resuscitation (CPR), the partial pressure of end-tidal carbon dioxide (PetCO₂) correlates with cardiac output and, consequently, it has a prognostic value in CPR. This study was undertaken to compare the initial PetCO₂ and the PetCO₂ after 1 min during CPR in asphyxial cardiac arrest versus primary cardiac arrest.MethodsThe prospective observational study included two groups of patients: cardiac arrest due to asphyxia with initial rhythm asystole or pulseless electrical activity, and cardiac arrest due to acute myocardial infarction or malignant arrhythmias with initial rhythm ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). The PetCO₂ was measured for both groups immediately after intubation and then repeatedly every minute, both for patients with and without return of spontaneous circulation (ROSC).ResultsWe analyzed 44 patients with asphyxial cardiac arrest and 141 patients with primary cardiac arrest. The first group showed no significant difference in the initial value of the PetCO₂, even when we compared those with and without ROSC. There was a significant difference in the PetCO₂ after 1 min of CPR between those patients with ROSC and those without ROSC. The mean value for all patients was significantly higher in the group with asphyxial arrest. In the group with VF/VT arrest there was a significant difference in the initial PetCO₂ between patients without and with ROSC. In all patients with ROSC the initial PetCO₂ was higher than 10 mmHg.ConclusionsThe initial PetCO₂ is significantly higher in asphyxial arrest than in VT/VF cardiac arrest. Regarding asphyxial arrest there is also no difference in values of initial PetCO₂ between patients with and without ROSC. On the contrary, there is a significant difference in values of the initial PetCO₂ in the VF/VT cardiac arrest between patients with and without ROSC. This difference could prove to be useful as one of the methods in prehospital diagnostic procedures and attendance of cardiac arrest. For this reason we should always include other clinical and laboratory tests.     

Brain tissue oxygen pressure and cerebral metabolism in an animal model of cardiac arrest and cardiopulmonary resuscitation

OBJECTIVE: Direct measurement of brain tissue oxygenation (PbtO2) is established during spontaneous circulation, but values of PbtO2 during and after cardiopulmonary resuscitation (CPR) are unknown. The purpose of this study was to investigate: (1) the time-course of PbtO2 in an established model of CPR, and (2) the changes of cerebral venous lactate and S-100B. METHODS: In 12 pigs (12-16 weeks, 35-45 kg), ventricular fibrillation (VF) was induced electrically during general anaesthesia. After 4 min of untreated VF, all animals were subjected to CPR (chest compression rate 100/min, FiO2 1.0) with vasopressor therapy after 7, 12, and 17 min (vasopressin 0.4, 0.4, and 0.8 U/kg, respectively). Defibrillation was performed after 22 min of cardiac arrest. After return of spontaneous circulation (ROSC), the pigs were observed for 1h. RESULTS: After initiation of VF, PbtO2 decreased compared to baseline (mean +/- SEM; 22 +/- 6 versus 2 +/- 1 mmHg after 4 min of VF; P < 0.05). During CPR, PbtO2 increased, and reached maximum values 8 min after start of CPR (25 +/- 7 mmHg; P < 0.05 versus no-flow). No further changes were seen until ROSC. Lactate, and S-100B increased during CPR compared to baseline (16 +/- 2 versus 85 +/- 8 mg/dl, and 0.46 +/- 0.05 versus 2.12 +/- 0.40 microg/l after 13 min of CPR, respectively; P < 0.001); lactate remained elevated, while S-100B returned to baseline after ROSC. CONCLUSIONS: Though PbtO2 returned to pre-arrest values during CPR, PbtO2 and cerebral lactate were lower than during post-arrest reperfusion with 100% oxygen, which reflected the cerebral low-flow state during CPR. The transient increase of S-100B may indicate a disturbance of the blood-brain-barrier.     

Fluid therapy and acute kidney injury in cardiogenic shock after cardiac arrest

Aim of the study

It has recently been suggested that acute kidney injury (AKI) may strongly be influenced by post-resuscitation disease and cardiogenic shock (CS), and may not just be a consequence of cardiac arrest and time without spontaneous circulation. AKI also has been suggested as a strong independent predictor of in-hospital mortality. Therefore the present study aimed at investigating the effect of fluid management on the incidence of AKI in patients with cardiogenic shock after cardiac arrest treated by mild therapeutic hypothermia.

Methods

Fluid therapy and the incidence of acute kidney injury (AKI) was retrospectively reviewed in 51 patients with cardiogenic shock after cardiac arrest comparing patients with and without hemodynamic (PPV, SVV) and volumetric (ELWI, GEDI) monitoring.

Results

There was no significant difference in baseline or cardiac arrest characteristics between hemodynamic monitored patients and conventional monitored patients. 28 patients were monitored by standard monitoring, in 23 patients monitoring was complemented by a PICCO system. In the first 24 h of treatment the total amount of fluid was significantly higher in patients under PICCO monitoring compared to conventional monitoring (4375 ± 1285 ml vs. 5449 ± 1438 ml, p = 0.007). This was associated with a significant reduction in the incidence of AKI (RIFLE ‘I’/‘F’: PICCO-group: 1 (4.3%) vs. conventional group 8 (28.6%), p = 0.03).

Conclusion

The presented data suggest that volume therapy guided by volumetric (ELWI, GEDI) and arterial waveform derived variables (PPV, SVV) can reduce the incidence of AKI in patients with cardiogenic shock after cardiac arrest treated with mild therapeutic hypothermia.     

The prevalence of bacteremia in out of hospital cardiac arrest patients presenting to the emergency department of a tertiary care hospital

BackgroundOut-of-hospital cardiac arrest (OHCA) remains one of the most common causes of death. There is a scarcity of evidence concerning the prevalence of bacteraemia in cardiac arrest patients presenting to the Emergency Department (ED). We aimed to determine the prevalence of bacteraemia in OHCA patients presenting to the ED, as well as study the association between bacteraemia and in-hospital mortality in OHCA patients. In addition, the association between antibiotic use during resuscitation and in-hospital mortality was examined.Methods and resultsThis was a study of 200 adult OHCA patients who presented to the ED between 2015 and 2019. Bacteraemia was confirmed if at least one of the blood culture bottles grew a non-skin flora pathogen or if two blood culture bottles grew a skin flora pathogen from two different sites. The prevalence of bacteraemia was 46.5%. Gram positive bacteria, specifically Staphylococcus species, were the most common pathogens isolated from the bacteremic group. 42 patients survived to hospital admission. The multivariate analysis revealed that there was no association between bacteraemia and hospital mortality in OHCA patients (OR = 1.3, 95% CI= 0.2–9.2) with a p-value of .8. There was no association between antibiotic administration during resuscitation and hospital mortality (OR = 0.6, 95% CI= 0.1 − 3.8) with a p-value of .6.ConclusionIn our study, the prevalence of bacteraemia among OHCA patients presenting to the ED was found to be 46.5%. Bacteremic and non-bacteremic OHCA patients had similar initial baseline characteristics and laboratory parameters except for higher serum creatinine and BUN in the bacteremic group. In OHCA patients who survived their ED stay there was no association between hospital mortality and bacteraemia or antibiotic administration during resuscitation. There is a need for randomised controlled trials with a strong patient oriented primary outcome to better understand the association between in-hospital mortality and bacteraemia or antibiotic administration in OHCA patients.

KEY MESSAGES

• We aimed to determine the prevalence of bacteraemia in OHCA patients presenting to the Emergency Department. In our study, we found that 46.5% of patients presenting to our ED with OHCA were bacteremic.
• Bacteremic and non-bacteremic OHCA patients had similar initial baseline characteristics and laboratory parameters except for higher serum creatinine and BUN in the bacteremic group.
• We found no association between bacteraemia and hospital mortality. There was no association between antibiotic administration during resuscitation and hospital mortality.
• There is a need for randomised controlled trials with a strong patient oriented primary outcome to better understand the association between in-hospital mortality and bacteraemia or antibiotic administration in OHCA patients.

     

Effectiveness of sepsis bundle application in cirrhotic patients with septic shock: a single-center experience

Purpose

To evaluate the effect of adherence to evidence-based guidelines of the Surviving Sepsis Campaign (SSC) on the outcome of cirrhotic patients with septic shock admitted to the intensive care unit.

Methods

This prospective observational cohort study included 38 patients with documented liver cirrhosis and septic shock admitted to a multidisciplinary intensive care unit at a University Hospital from January 2005 to June 2009. In each patient, the compliance to 4 resuscitation (ie, 6-hour bundle) and to 3 management (i.e. 24-hour bundle) interventions recommended by the SSC guidelines and the 30-day mortality were measured.

Results

The 6-hour, 24-hour, and all bundles were completed in 50 %, 52%, and 39% of the patients, respectively. The characteristics at admission and the 30-day mortality of patients with all-bundle compliance (n = 15; mortality 86.6%) were similar to those of patients without bundle compliance (n = 23; mortality 78.2%), except for central venous O₂ saturation. Unadjusted and adjusted regression analysis showed that none of the single sepsis interventions and bundles were independently associated with 30-day mortality.

Conclusions

In our observational study, the adherence to the interventions recommended by the SSC evidence-based guidelines did not provide an improvement in the survival rate of cirrhotic patients with septic shock.     

Correlations between hemodynamic, oxygenation and tissue perfusion parameters during asphyxial cardiac arrest and resuscitation in a pediatric animal model

Aim

To analyze the correlations between hemodynamic, oxygenation and tissue perfusion values in an infant animal model of asphyctic cardiac arrest (ACA).

Methods

A prospective observational animal study was performed in seventy one, two month-old piglets. CA was induced by removal of mechanical ventilation and was followed by advanced life support after at least 10 min. Correlations between hemodynamic [heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI) and intrathoracic blood index (ITBI) measured by PiCCO method], blood gas values (arterial and central venous saturation), and tissue perfusion values [intramucosal gastric pH (pHi), and tissue oxygenation (cerebral and renal saturation)] were analyzed during asphyxia, resuscitation and after return of spontaneous circulation (ROSC).

Results

Among global hemodynamic parameters, the only moderate significant correlation observed was between CI and ITBI (r = .551). Among tissue oxygenation/perfusion values, a moderate to good significant correlation (r = .460-.763) between arterial oxygen saturation, central venous, renal and cerebral oxygen saturation was observed. Lactic acid, potassium (K) and pHi were correlated (r = .561-.639), but no correlation was found between them and tissue oxygenation parameters. Global hemodynamic parameters (CI, HR, MAP) did not correlate with renal and cerebral saturations and tissue perfusion parameters.

Conclusions

During ACA and after ROSC global hemodynamic parameters do not correlate with oxygenation and tissue perfusion values. Additional studies which assess the potential usefulness of tissue oxygenation/perfusion parameters during cardiac arrest and ROSC are needed.     

The effect of team-based CPR on outcomes in out of hospital cardiac arrest patients: A meta-analysis

Objectives

The objective of this systematic review and meta-analysis was to determine the effects of team cardiopulmonary resuscitation (CPR) on outcomes of patients with out-of-hospital cardiac arrest (OHCA).

The influence of age and chronic medical conditions on neurological outcomes in out of hospital cardiac arrest

AimIt is unknown whether older patients with out of hospital cardiac arrest (OHCA) have worse outcomes because of aging itself, or because age can be a marker for overall health status. We aimed to study the prognostic utility of age and pre-arrest comorbidities.MethodsWe conducted a retrospective cohort study, reviewing electronic health records of all adults treated for non-traumatic OHCA in the University of Michigan Emergency Department (N = 588). Primary covariates included age, Charlson Comorbidity Index (CCI), and a combined Charlson-age index. The primary dichotomized outcome was favorable neurological outcome (cerebral performance category, 1–2), evaluated by logistic regressions.ResultsDementia (p = 0.01), witnessed arrest (p = 0.03), bystander CPR (p < 0.001), presenting rhythm (p < 0.001), and mild therapeutic hypothermia (p < 0.001) were associated with the primary outcome. Increasing age (unadjusted OR for each decade of life, 95% CI: 0.78, 0.70–0.88; adjusted 0.79, 0.67–0.94) was negatively associated with likelihood of a favorable neurological outcome. CCI and combined Charlson-age index significantly predicted outcome in the unadjusted, but not adjusted analysis. Composite variables were stronger predictors in patients with shockable than non-shockable presenting rhythms (interaction terms: age and rhythm [p = 0.004], CCI and rhythm [p = 0.01]).ConclusionAge, but not CCI, was significantly associated with less favorable neurological outcomes in patients with OHCA after adjusting important covariates. Age appears to be an independent predictor of prognosis rather than a marker for comorbidity.     

Hyperoxic ventilation improves survival in pigs during endotoxaemia at the critical hemoglobin concentration

Aim of the study

Recently it has been demonstrated that short term hyperoxic ventilation (HV) can improve glucose metabolism, reduce pulmonary and hepatic apoptosis, and improve gastrointestinal perfusion during acute sepsis. However, it is unknown whether additional O₂ improves survival. Therefore we investigated the effects of increased plasma O₂ on survival during extreme anaemia and concomitant endotoxaemia in order to quantify the efficacy of HV.

Methods

Endotoxaemia (Salmonella abortus equi-LPS) was induced in 14 anesthetized pigs ventilated with room air (FiO₂ = 0.21). Simultaneously, animals were haemodiluted by exchange of whole blood for 6% hydroxyethyl starch (200,000:0.5) until the individual critical hemoglobin concentration (Hb_crit) was achieved (outermost limit of tissue oxygenation). Subsequently, animals were either ventilated with an FiO₂ of 0.21 (NOX, n = 7) or an FiO₂ of 1.0 (HOX, n = 7), and observed thereafter for 6 h without further intervention.

Results

HV significantly prolonged survival time at Hb_crit (NOX, 30 [27/35] min; HOX, 172 [111/235] min, p < 0.05). In contrast to the NOX group, HV maintained MAP, and improved DO₂ and tissue oxygenation in the HOX group.

Conclusion

The improvement of survival, oxygen transport and tissue oxygenation seems to underline the efficacy of HV during endotoxaemia and concomitant acute anaemia. Further studies are needed to transfer these results into daily clinical practice.     

The association of gasping and outcome,in out of hospital cardiac arrest: A systematic review and meta-analysis

ObjectiveGasping is common after cardiac arrest, and its frequency decreases over time. The aim of this study was to conduct a meta-analysis to evaluate the association of gasping and survival to discharge in patients who suffered out-of-hospital cardiac arrest.MethodsRelevant studies were identified by searching in PubMed, Medline, Embase, OVID, Web of Science and Google Scholar. Risk ratios (RR) and 95% confidence intervals (CI) were calculated to assess the association of gasping and on out-of-hospital cardiac arrest outcomes. Heterogeneity, subgroup analysis, sensitivity analysis and publication bias were explored.ResultsIndividual patient data was obtained from 10,797 participants suffered out-of-hospital cardiac arrest in five cohort studies of 4 articles. A fixed effects model suggested that patients with gasping were 3.525 times (95% CI: 3.028–4.104; P < 0.01) more likely to survive to discharge than those without gasping, and there was no heterogeneity among studies (P = 0.564). Also it may be a favorable factor for return of spontaneous circulation (RR: 2.170; 95% CI: 1.691, 2.785) with high heterogeneity (Q = 5.26; P = 0.022).ConclusionsFindings of this meta-analysis demonstrated that gasping is common after cardiac arrest, and is associated with increased survival to discharge. Patients who are cardiac arrest with gasping should be promptly resuscitated.     

近红外光谱测量脑血氧饱和度与成人心脏骤停后接受目标体温管理患者神经系统预后的关系:系统评价和荟萃分析

目的研究脑血氧饱和度(rSO₂)在心脏骤停后综合征(PCAS)昏迷患者的目标体温管理(TTM)期间预测神经系统预后的作用。方法本研究根据PRISMA指南进行报告,检索了Pubmed、Embase、Cochane Library、Web of science、Google Scholar、Clinical gov、万方、维普、CNKI共9个数据库。除外研究类型为病例报告、综述和研究样本量小于5例的研究,收集所有在成人心脏骤停(CA)期间进行近红外光谱(NIRS)测量的研究。两名审稿人评估纳入文章的质量并提取数据。结果效应使用标准化平均差(SMD)进行标准化。结果本荟萃分析纳入11项研究,其中2项为随机对照研究,9项为观察性研究。共计681例患者。患者TTM期间NIRS测量的rSO₂值在TTM 24 h(低温结束)、TTM 24~36 h(复温阶段)和TTM 36~48 h(初始常温阶段)与神经系统预后相关(TTM 24 h:SMD=0.45,95%CI 0.29~0.61;TTM 24~36 h:SMD=1.17,95%CI 0.85~1.50;TTM 36~48 h:SMD=0.26,95%CI 0.10~0.43),良好的神经系统预后(CPC 1~2)组具有较高的rSO₂值。在TTM开始时、TTM期间和TTM 72 h的常温阶段,均未发现NIRS测量的rSO₂值与神经系统预后的相关性。结论对于行TTM的CA患者,在TTM 24~48 h期间良好神经系统预后患者NIRS测量的rSO₂值高于神经系统预后不良的患者,其中TTM 24~36 h(复温阶段)与良好神经系统预后有较强的关联。     

Effect of moderate hyperventilation and induced hypertension on cerebral tissue oxygenation after cardiac arrest and therapeutic hypothermia

Aim

Improving cerebral perfusion is an essential component of post-resuscitation care after cardiac arrest (CA), however precise recommendations in this setting are limited. We aimed to examine the effect of moderate hyperventilation (HV) and induced hypertension (IH) on non-invasive cerebral tissue oxygenation (SctO₂) in patients with coma after CA monitored with near-infrared spectroscopy (NIRS) during therapeutic hypothermia (TH).

Methods

Prospective pilot study including comatose patients successfully resuscitated from out-of-hospital CA treated with TH, monitored with NIRS. Dynamic changes of SctO₂ upon HV and IH were analyzed during the stable TH maintenance phase. HV was induced by decreasing PaCO₂ from ∼40 to ∼30 mmHg, at stable mean arterial blood pressure (MAP ∼ 70 mmHg). IH was obtained by increasing MAP from ∼70 to ∼90 mmHg with noradrenaline.

Results

Ten patients (mean age 69 years; mean time to ROSC 19 min) were studied. Following HV, a significant reduction of SctO₂ was observed (baseline 74.7 ± 4.3% vs. 69.0 ± 4.2% at the end of HV test, p < 0.001, paired t-test). In contrast, IH was not associated with changes in SctO₂ (baseline 73.6 ± 3.5% vs. 74.1 ± 3.8% at the end of IH test, p = 0.24).

Conclusions

Moderate hyperventilation was associated with a significant reduction in SctO₂, while increasing MAP to supra-normal levels with vasopressors had no effect on cerebral tissue oxygenation. Our study suggests that maintenance of strictly normal PaCO₂ levels and MAP targets of 70 mmHg may provide optimal cerebral perfusion during TH in comatose CA patients.     

Perfluorocarbon induced intra-arrest hypothermia does not improve survival in a swine model of asphyxial cardiac arrest

Background

Pulseless electrical activity is an important cause of cardiac arrest. Our purpose was to determine if induction of hypothermia with a cold perfluorocarbon-based total liquid ventilation (TLV) system would improve resuscitation success in a swine model of asphyxial cardiac arrest/PEA.

Methods

Twenty swine were randomly assigned to control (C, no ventilation, n = 11) or TLV with pre-cooled PFC (n = 9) groups. Asphyxia was induced by insertion of a stopper into the endotracheal tube, and continued in both groups until loss of aortic pulsations (LOAP) was reached, defined as a pulse pressure less than 2 mmHg. The TLV animals underwent asphyxial arrest for an additional 2 min after LOAP, followed by 3 min of hypothermia, prior to starting CPR. The C animals underwent 5 min of asphyxia beyond LOAP. Both groups then underwent CPR for at least 10 min. The endpoint was the resumption of spontaneous circulation maintained for 10 min.

Results

Seven of 9 animals achieved resumption of spontaneous circulation (ROSC) in the TLV group vs. 5 of 11 in the C group (p = 0.2). The mean pulmonary arterial temperature was lower in total liquid ventilation animals starting 4 min after induction of hypothermia (TLV 36.3 ± 0.2 °C vs. C 38.1 ± 0.2 °C, p < 0.0001). Arterial pO₂ was higher in total liquid ventilation animals at 2.5 min of CPR (TLV 76 ± 12 mmHg vs. C 44 ± 2 mmHg; p = 0.03).

Conclusion

Induction of moderate hypothermia using perfluorocarbon-based total liquid ventilation did not improve ROSC success in this model of asphyxial cardiac arrest.     

Arterial minus end-tidal CO2 as a prognostic factor of hospital survival in patients resuscitated from cardiac arrest

AIMS: The purpose of this study was to determine the clinical value of arterial minus end-tidal CO(2) [P(a-et)CO(2)] and alveolar dead space ventilation ratio (V(dA)/V(t)) as indicators of hospital mortality in patients that have been resuscitated from cardiac arrest at emergency department. MATERIALS AND METHODS: Forty-four patients with a return of spontaneous circulation (ROSC) after cardiac arrest were studied in the emergency department of a university teaching hospital from March 2004 to February 2006. Mean arterial pressure (MAP), serum lactate, arterial blood gas studies, end-tidal CO(2) (EtCO(2)), P(a-et)CO(2), and V(dA)/V(t) were evaluated at 1 h after ROSC. We compared these variables between hospital survivors and non-survivors. RESULTS: The rates of ventricular fibrillation and pulseless ventricular tachycardia in hospital survivors were higher than those of non-survivors (53.0 and 9.7%, respectively, p=0.002). Hospital survivors had significantly higher MAP, lower serum lactate, lower P(a-et)CO(2), and lower V(dA)/V(t) value than non-survivors. Receiver operator characteristic (ROC) curves of serum lactate, P(a-et)CO(2), and V(dA)/V(t) showed significant sensitivity and specificity for hospital mortality. Specifically, lactate > or = 10.0 mmol/L, P(a-et)CO(2) > or = 12.5 mmHg, and V(dA)/V(t) > or = 0.348 were all associated with high hospital mortality (p=0.000, 0.001 and 0.000, respectively). CONCLUSIONS: This study showed that high serum lactate, high P(a-et)CO(2) and high V(dA)/V(t) during early ROSC in cardiac arrest patients suggest high hospital mortality. If future studies validate this model, the P(a-et)CO(2) and V(dA)/V(t) may provide useful guidelines for the early post-resuscitation care of cardiac arrest patients in emergency departments.     

A feasibility study of cerebral oximetry monitoring during the post-resuscitation period in comatose patients following cardiac arrest

Background

One of the major causes of death and neurological injury after cardiac arrest is delayed ischemia combined with oxygen free radical mediated reperfusion injury. Consequently determining the optimal balance between oxygen delivery and uptake in the brain using a reliable non-invasive monitoring system during the post-resuscitation period is of importance. In this observational study, we evaluated the feasibility of using cerebral oximetry during the post-resuscitation period in order to identify changes in regional cerebral oxygen saturation (rSO₂) and its association with survival to discharge.

Methods

21 consecutive patients admitted to the intensive care units following cardiac arrest had cerebral oximetry monitoring carried out for 48 h. Mean rSO₂ values were collected during the first 24 h and then again during the subsequent 24–48 h of the post-resuscitation period.

Results

43% (n = 9) patients survived to hospital discharge and 57% (n = 12) died. Amongst all patients the median (IQR) rSO₂% was 65.5% (62.6–68.2) in the first 24-h following ROSC and increased to 72.1% (64.6–73.7) (p = 0.11) in the subsequent 24–48 h. The median (IQR) rSO₂% during the first 24 h in patients who survived to discharge compared to those who did not survive were significantly higher 68.2% (66.0–71.0) vs. 62.9% (56.5–66.0), p = 0.01). During the subsequent 24–48 h period, while a difference in the rSO₂ between survivors and non-survivors was noted, this did not achieve statistical significance (median (IQR): 73.7 (70.2–74.0) vs. 66.5 (58.2–72.1), p = 0.11).

Conclusions

Our study indicates that the use of cerebral oximetry is feasible during the post resuscitation period after cardiac arrest. Further studies are needed to determine whether cerebral oximetry may be used as a novel non-invasive monitoring system to evaluate changes in the balance between cerebral oxygen delivery and uptake during the post-resuscitation period.     

Effects of cerebral hypoperfusion on bispectral index: A randomised, controlled animal experiment during haemorrhagic shock

Background

The aim of this porcine haemorrhagic shock model was to investigate the changes of bispectral index (BIS) after slow and fast recovery of cerebral perfusion, and its correlation with plasma propofol concentrations.

Methods

After Animal Investigational Committee approval, 16 pigs during propofol anaesthesia underwent a liver trauma with severe hypotension, and were randomly assigned to receive therapy for either slow recovery (fluid resuscitation; slow group; n = 8) or fast recovery of cerebral perfusion (vasopressor combined with hypertonic-saline-starch; fast group; n = 8), respectively. Cerebral perfusion pressure (CPP = MAP − ICP), cerebral tissue oxygenation index (TOI), BIS, and plasma concentrations of propofol and haemoglobin were measured at baseline (Pre-shock), haemodynamic decompensation (Shock), and 5 (Therapy) and 30 min (End) after therapy, respectively.

Results

CPP, TOI, and BIS decreased significantly during shock (pre-shock vs. shock, fast: CPP: 65 ± 14 vs. 15 ± 4 mm Hg; TOI: 64 ± 6 vs. 47 ± 7%; BIS 60 ± 5 vs. 9 ± 10; slow: CPP: 60 ± 12 vs. 13 ± 7 mm Hg; TOI: 68 ± 7 vs. 49 ± 7%; BIS 63 ± 5 vs. 13 ± 12; P < 0.05). In the fast group, CPP, TOI, and BIS increased after therapy compared to the slow group (Therapy, fast: CPP: 47 ± 15 mm Hg, TOI: 61 ± 7%, BIS: 47 ± 21; slow: CPP: 18 ± 9 mm Hg, TOI: 51 ± 5%, BIS: 21 ± 19; P < 0.05). Propofol and haemoglobin concentrations were comparable between groups throughout the resuscitation phase.

Conclusions

In a haemorrhagic shock scenario, therapies with different impact on cerebral perfusion resulted in differing changes of BIS values, while plasma propofol and haemoglobin concentrations were comparable during the resuscitation phase; this suggests that BIS may also have reflected changes of cerebral perfusion.     

The cellular and molecular origin of reactive oxygen species generation during myocardial ischemia and reperfusion

Myocardial ischemia-reperfusion injury is an important cause of impaired heart function in the early postoperative period subsequent to cardiac surgery. Reactive oxygen species (ROS) generation increases during both ischemia and reperfusion and it plays a central role in the pathophysiology of intraoperative myocardial injury. Unfortunately, the cellular source of these ROS during ischemia and reperfusion is often poorly defined. Similarly, individual ROS members tend to be grouped together as free radicals with a uniform reactivity towards biomolecules and with deleterious effects collectively ascribed under the vague umbrella of oxidative stress. This review aims to clarify the identity, origin, and progression of ROS during myocardial ischemia and reperfusion. Additionally, this review aims to describe the biochemical reactions and cellular processes that are initiated by specific ROS that work in concert to ultimately yield the clinical manifestations of myocardial ischemia-reperfusion. Lastly, this review provides an overview of several key cardioprotective strategies that target myocardial ischemia-reperfusion injury from the perspective of ROS generation. This overview is illustrated with example clinical studies that have attempted to translate these strategies to reduce the severity of ischemia-reperfusion injury during coronary artery bypass grafting surgery.     

Effects of recombinant-hemoglobin solutions rHb2.0 and rHb1.1 on blood pressure, intestinal blood flow, and gut oxygenation in a rat model of hemorrhagic shock

The vasoconstriction induced by hemoglobin-based oxygen carriers (HBOCs), mainly a result of nitric oxide (NO) scavenging, until now has limited the application of HBOCs as resuscitation fluids. In this study, we tested the hypothesis that the new modified recombinant-hemoglobin solution rHb2.0, with a 20 to 30 times lesser NO-scavenging rate, would minimize vasoconstriction without adverse effects on microvascular oxygenation. Responses were compared with those to rHb1.1, a recombinant-hemoglobin solution with a wild-type NO-scavenging rate, as well as an oncotically matched albumin solution. In a fixed-pressure (40 mm Hg) rat model of hemorrhagic shock and resuscitation, rHb2.0 and albumin both restored mean arterial pressure (MAP) to baseline values, whereas rHb1.1 increased MAP to 27% above the baseline value. Mesenteric vascular resistance after resuscitation with rHb2.0 was 57% less than that with rHb1.1. rHb2.0 was found to have 55% greater intestinal oxygen delivery (Do2int ) and resulted in a 27% lower oxygen-extraction rate than did rHb1.1 after resuscitation. Intestinal microvascular Po2 , determined on the basis of oxygen-dependent quenching of palladium-porphyrin phosphorescence, revealed no difference between rHb2.0 and rHb1.1. The findings of this study confirm that the well-known pressure effect of HBOCs is caused by their effect on the NO-scavenging rate; recombinant modification of this rate did not increase MAP during resuscitation compared with baseline values. Although systemic vasoconstriction was absent, intestinal vasoconstriction almost negligible, and Do2int greater after resuscitation with rHb2.0, the effect of rHb2.0 on pH, base-excess and microvascular Po2 levels after resuscitation were comparable to those achieved with the use of the albumin solution.     

Temporal trends (2002–2014) of incidence and shockable status of adult emergency medical service attended out‐of‐hospital cardiac arrest of presumed cardiac aetiology in Queensland

Objective

To describe trends in incidence and shockable status of adult out‐of‐hospital cardiac arrest (OHCA) of presumed cardiac aetiology attended by Queensland Ambulance Service (QAS) paramedics between 2002 and 2014.

Methods

The QAS cardiac arrest registry was used to collect data. Analyses included age‐standardised rates by gender for all adults and older adults only (65 years+); age‐specific incidence rates of young adults (18–49), middle age adults (50–64) and five groups of older adults (65–69, 70–74, 75–79, 80–84 and 85+); and proportions of shockable versus non‐shockable initial rhythm together and by age group (young, middle age and older adults). Temporal trends were analysed.

Results

Over the 13 years, 32 346 cases of adult OHCA of presumed cardiac aetiology were recorded on the QAS OHCA registry. Age‐standardised incidence reduced significantly over time overall and in males only, in all adults and independently in older adults. A significant reduction independently in females was observed only in older adults. Age‐specific rates reduced in the 18–49, 70–74, 75–79 and 80–84 year age groups, increased in the 50–64 age group (largely attributable to females) and no significant trends were found in the 65–69 and 85+ age groups. The proportion of cases with an initially shockable rhythm significantly decreased overall. This trend was observed independently in older adults, but not in young or middle age adults.

Conclusion

Age‐standardised incidence has reduced with a period of stagnation in the middle age and early older years. These factors require consideration in data interpretation and strategy planning.