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1.
Int J Angiol ; 30(4): 310-312, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34849111

RESUMO

In this case report we describe a novel and successful revascularization approach in instances of allograft and distal limb ischemia after kidney transplantation. Stenosis proximal to transplant renal artery anastomoses is a complication leading to allograft dysfunction and/or loss. We present a femorofemoral bypass graft with ringed polytetrafluoroethylene (PTFE). In this occasion, revascularization was achieved by a backflow mechanism. The approach described achieved its goal of revascularizing the allograft as well as the distal extremity, with both short- and long-term successful outcomes. Benefits of this approach when compared with re-implantation or procedures directly involving the transplant renal artery include minimization of ischemic time, no need to repair the stenosis, anastomoses with vessels of greater diameter, no need to perfuse the kidney, no need to take down the renal artery anastomosis, no need to dissect the transplanted kidney, and no further lower extremity ischemia. This approach does not require any proximal temporary inflow occlusion (as seen with stent placement) or clamping of the arterial inflow to the kidney. This procedure was completed without having to infuse any preservation fluid into the kidney.

3.
J Transl Med ; 19(1): 462, 2021 Nov 16.
Artigo em Inglês | MEDLINE | ID: mdl-34781966

RESUMO

BACKGROUND: Despite the benefits of extracorporeal cardiopulmonary resuscitation (ECPR) in cohorts of selected patients with cardiac arrest (CA), extracorporeal membrane oxygenation (ECMO) includes an artificial oxygenation membrane and circuits that contact the circulating blood and induce excessive oxidative stress and inflammatory responses, resulting in coagulopathy and endothelial cell damage. There is currently no pharmacological treatment that has been proven to improve outcomes after CA/ECPR. We aimed to test the hypothesis that administration of hydrogen gas (H2) combined with ECPR could improve outcomes after CA/ECPR in rats. METHODS: Rats were subjected to 20 min of asphyxial CA and were resuscitated by ECPR. Mechanical ventilation (MV) was initiated at the beginning of ECPR. Animals were randomly assigned to the placebo or H2 gas treatment groups. The supplement gas was administered with O2 through the ECMO membrane and MV. Survival time, electroencephalography (EEG), brain functional status, and brain tissue oxygenation were measured. Changes in the plasma levels of syndecan-1 (a marker of endothelial damage), multiple cytokines, chemokines, and metabolites were also evaluated. RESULTS: The survival rate at 4 h was 77.8% (7 out of 9) in the H2 group and 22.2% (2 out of 9) in the placebo group. The Kaplan-Meier analysis showed that H2 significantly improved the 4 h-survival endpoint (log-rank P = 0.025 vs. placebo). All animals treated with H2 regained EEG activity, whereas no recovery was observed in animals treated with placebo. H2 therapy markedly improved intra-resuscitation brain tissue oxygenation and prevented an increase in central venous pressure after ECPR. H2 attenuated an increase in syndecan-1 levels and enhanced an increase in interleukin-10, vascular endothelial growth factor, and leptin levels after ECPR. Metabolomics analysis identified significant changes at 2 h after CA/ECPR between the two groups, particularly in D-glutamine and D-glutamate metabolism. CONCLUSIONS: H2 therapy improved mortality in highly lethal CA rats rescued by ECPR and helped recover brain electrical activity. The underlying mechanism might be linked to protective effects against endothelial damage. Further studies are warranted to elucidate the mechanisms responsible for the beneficial effects of H2 on ischemia-reperfusion injury in critically ill patients who require ECMO support.

4.
J Transl Med ; 19(1): 390, 2021 Nov 14.
Artigo em Inglês | MEDLINE | ID: mdl-34774068

RESUMO

BACKGROUND: Despite much evidence supporting the monitoring of the divergence of transcutaneous partial pressure of carbon dioxide (tcPCO2) from arterial partial pressure carbon dioxide (artPCO2) as an indicator of the shock status, data are limited on the relationships of the gradient between tcPCO2 and artPCO2 (tc-artPCO2) with the systemic oxygen metabolism and hemodynamic parameters. Our study aimed to test the hypothesis that tc-artPCO2 can detect inadequate tissue perfusion during hemorrhagic shock and resuscitation. METHODS: This prospective animal study was performed using female pigs at a university-based experimental laboratory. Progressive massive hemorrhagic shock was induced in mechanically ventilated pigs by stepwise blood withdrawal. All animals were then resuscitated by transfusing the stored blood in stages. A transcutaneous monitor was attached to their ears to measure tcPCO2. A pulmonary artery catheter (PAC) and pulse index continuous cardiac output (PiCCO) were used to monitor cardiac output (CO) and several hemodynamic parameters. The relationships of tc-artPCO2 with the study parameters and systemic oxygen delivery (DO2) were analyzed. RESULTS: Hemorrhage and blood transfusion precisely impacted hemodynamic and laboratory data as expected. The tc-artPCO2 level markedly increased as CO decreased. There were significant correlations of tc-artPCO2 with DO2 and COs (DO2: r = - 0.83, CO by PAC: r = - 0.79; CO by PiCCO: r = - 0.74; all P < 0.0001). The critical level of oxygen delivery (DO2crit) was 11.72 mL/kg/min according to transcutaneous partial pressure of oxygen (threshold of 30 mmHg). Receiver operating characteristic curve analyses revealed that the value of tc-artPCO2 for discrimination of DO2crit was highest with an area under the curve (AUC) of 0.94, followed by shock index (AUC = 0.78; P < 0.04 vs tc-artPCO2), and lactate (AUC = 0.65; P < 0.001 vs tc-artPCO2). CONCLUSIONS: Our observations suggest the less-invasive tc-artPCO2 monitoring can sensitively detect inadequate systemic oxygen supply during hemorrhagic shock. Further evaluations are required in different forms of shock in other large animal models and in humans to assess its usefulness, safety, and ability to predict outcomes in critical illnesses.

5.
Sci Rep ; 11(1): 19652, 2021 Oct 04.
Artigo em Inglês | MEDLINE | ID: mdl-34608241

RESUMO

Traumatic peri-contusional penumbra represents crucial targets for therapeutic interventions after traumatic brain injury (TBI). Current resuscitative approaches may not adequately alleviate impaired cerebral microcirculation and, hence, compromise oxygen delivery to peri-contusional areas. Low-frequency oscillations in cerebral blood flow (CBF) may improve cerebral oxygenation in the setting of oxygen deprivation. However, no method has been reported to induce controllable oscillations in CBF and it hasn't been applied as a therapeutic strategy. Electrical stimulation of the trigeminal nerve (TNS) plays a pivotal role in modulating cerebrovascular tone and cerebral perfusion. We hypothesized that TNS can modulate CBF at the targeted frequency band via the trigemino-cerebrovascular network, and TNS-induced CBF oscillations would improve cerebral oxygenation in peri-contusional areas. In a rat model of TBI complicated by hemorrhagic shock, TNS-induced CBF oscillations conferred significant preservation of peri-contusional tissues leading to reduced lesion volume, attenuated hypoxic injury and neuroinflammation, increased eNOS expression, improved neurological recovery and better 10-day survival rate, despite not significantly increasing CBF as compared with those in immediate and delayed resuscitation animals. Our findings indicate that low-frequency CBF oscillations enhance cerebral oxygenation in peri-contusional areas, and play a more significant protective role than improvements in non-oscillatory cerebral perfusion or volume expansion alone.

6.
Sci Rep ; 11(1): 21124, 2021 10 26.
Artigo em Inglês | MEDLINE | ID: mdl-34702896

RESUMO

Patients with coronavirus disease 2019 (COVID-19) can have increased risk of mortality shortly after intubation. The aim of this study is to develop a model using predictors of early mortality after intubation from COVID-19. A retrospective study of 1945 intubated patients with COVID-19 admitted to 12 Northwell hospitals in the greater New York City area was performed. Logistic regression model using backward selection was applied. This study evaluated predictors of 14-day mortality after intubation for COVID-19 patients. The predictors of mortality within 14 days after intubation included older age, history of chronic kidney disease, lower mean arterial pressure or increased dose of required vasopressors, higher urea nitrogen level, higher ferritin, higher oxygen index, and abnormal pH levels. We developed and externally validated an intubated COVID-19 predictive score (ICOP). The area under the receiver operating characteristic curve was 0.75 (95% CI 0.73-0.78) in the derivation cohort and 0.71 (95% CI 0.67-0.75) in the validation cohort; both were significantly greater than corresponding values for sequential organ failure assessment (SOFA) or CURB-65 scores. The externally validated predictive score may help clinicians estimate early mortality risk after intubation and provide guidance for deciding the most effective patient therapies.


Assuntos
COVID-19/diagnóstico , COVID-19/mortalidade , Intubação Intratraqueal/métodos , Índice de Gravidade de Doença , Adolescente , Adulto , Fatores Etários , Idoso , Pressão Arterial , COVID-19/terapia , Feminino , Ferritinas/sangue , Humanos , Concentração de Íons de Hidrogênio , Masculino , Pessoa de Meia-Idade , New York , Nitrogênio/metabolismo , Oxigênio/metabolismo , Valor Preditivo dos Testes , Curva ROC , Análise de Regressão , Reprodutibilidade dos Testes , Estudos Retrospectivos , Sensibilidade e Especificidade , Vasoconstritores/farmacologia , Adulto Jovem
8.
Mol Med ; 27(1): 135, 2021 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-34689738

RESUMO

BACKGROUND: Cardiac arrest (CA) results in loss of blood circulation to all tissues leading to oxygen and metabolite dysfunction. Return of blood flow and oxygen during resuscitative efforts is the beginning of reperfusion injury and is marked by the generation of reactive oxygen species (ROS) that can directly damage tissues. The plasma serves as a reservoir and transportation medium for oxygen and metabolites critical for survival as well as ROS that are generated. However, the complicated interplay among various ROS species and antioxidant counterparts, particularly after CA, in the plasma have not been evaluated. In this study, we assessed the equilibrium between pro- and anti-oxidants within the plasma to assess the oxidative status of plasma post-CA. METHODS: In male Sprague-Dawley rats, 10 min asphyxial-CA was induced followed by cardiopulmonary resuscitation (CPR). Plasma was drawn immediately after achieving return of spontaneous circulation (ROSC) and after 2 h post-ROSC. Plasma was isolated and analyzed for prooxidant capacity (Amplex Red and dihydroethidium oxidation, total nitrate and nitrite concentration, xanthine oxidase activity, and iron concentration) and antioxidant capacity (catalase and superoxide dismutase activities, Total Antioxidant Capacity, and Iron Reducing Antioxidant Power Assay). The consequent oxidative products, such as 4-Hydroxyl-2-noneal, malondialdehyde, protein carbonyl, and nitrotyrosine were evaluated to determine the degree of oxidative damage. RESULTS: After CA and resuscitation, two trends were observed: (1) plasma prooxidant capacity was lower during ischemia, but rapidly increased post-ROSC as compared to control, and (2) plasma antioxidant capacity was increased during ischemia, but either decreased or did not increase substantially post-ROSC as compared to control. Consequently, oxidation products were increased post-ROSC. CONCLUSION: Our study evaluated the disbalance of pro- and anti-oxidants after CA in the plasma during the early phase after resuscitation. This disequilibrium favors the prooxidants and is associated with increased levels of downstream oxidative stress-induced end-products, which the body's antioxidant capacity is unable to directly mitigate. Here, we suggest that circulating plasma is a major contributor to oxidative stress post-CA and its management requires substantial early intervention for favorable outcomes.

9.
Curr Opin Crit Care ; 27(6): 656-662, 2021 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-34581299

RESUMO

PURPOSE OF REVIEW: To provide a framework for resuscitation of COVID-19 critical illness for emergency and intensive care clinicians with the most up to date evidence and recommendations in the care of COVID-19 patients in cardiac arrest or in extremis. RECENT FINDINGS: Performing cardiopulmonary resuscitation (CPR) on COVID-19 patients requires the clinicians to adopt infection mitigation strategies such as full personal protective equipment, mechanical chest compression devices, and restricting the number of people present during the resuscitation. The time of intubation is a subject of ongoing research and clinicians should use their best judgment for each patient. Clinicians should prepare for CPR in prone position. Particular attention should be given to the psychological well-being of the staff. Point of care ultrasound has proved to be an invaluable diagnostic tool in assessing ventricular dysfunction and parenchymal lung disease. Although novel therapies to supplant the function of diseased lungs have shown promise in select patients the evidence is still being collected. The end-of-life discussions have been negatively impacted by prognostic uncertainty as well as barriers to in person meetings with families. SUMMARY: The resuscitation of critically ill COVID-19 patients poses new challenges, but the principles remain largely unchanged.


Assuntos
COVID-19 , Reanimação Cardiopulmonar , Humanos , New York , Pandemias , SARS-CoV-2
10.
Resuscitation ; 2021 Sep 16.
Artigo em Inglês | MEDLINE | ID: mdl-34536559

RESUMO

BACKGROUND: The proportion of adult patients with return of spontaneous circulation (ROSC) following out-of-hospital cardiac arrest (OHCA) remains unchanged since 2012. A better resuscitation strategy is needed. This study evaluated the effectiveness of a regional cerebral oxygen saturation (rSO2)-guided resuscitation protocol without rhythm check based on our previous study. METHODS: Because defibrillation is the definitive therapy that should be performed without delay for shockable rhythm, the study subjects were OHCA patients with non-shockable rhythm on hospital arrival at three emergency departments. They were divided into three groups based on their baseline rSO2 value (%): ≥50, ≥40 to <50, or <40. Continuous chest compression without rhythm checks was performed for 16 minutes or until a maximum increase in rSO2 of 10%, 20%, or 35% was achieved in each group, respectively. This intervention cohort was compared with a historical control cohort regarding the probability of ROSC using inverse probability of treatment weighting (IPTW) with propensity score. RESULTS: The control and intervention cohorts respectively included 86 and 225 patients. The rate of ROSC was not significantly different between the groups (adjusted OR 0.91 [95% CI, 0.64-1.29], P = 0.60), but no serious adverse events occurred. Sensitivity analyses 1 and 2 showed a significant difference or positive tendency for higher probability of ROSC (adjusted OR 1.63 [95% CI, 1.22-2.17], P < 0.001) (adjusted OR 1.25 [95% CI, 0.95-1.63], P = 0.11). CONCLUSIONS: This trial suggested that a new cardiopulmonary resuscitation protocol with different rhythm check timing could be created using the rSO2 value. Clinical trial number: UMIN000025684.

11.
Lancet ; 398(10307): 1257-1268, 2021 10 02.
Artigo em Inglês | MEDLINE | ID: mdl-34454688

RESUMO

Cardiopulmonary resuscitation prioritises treatment for cardiac arrests from a primary cardiac cause, which make up the majority of treated cardiac arrests. Early chest compressions and, when indicated, a defibrillation shock from a bystander give the best chance of survival with a good neurological status. Cardiac arrest can also be caused by special circumstances, such as asphyxia, trauma, pulmonary embolism, accidental hypothermia, anaphylaxis, or COVID-19, and during pregnancy or perioperatively. Cardiac arrests in these circumstances represent an increasing proportion of all treated cardiac arrests, often have a preventable cause, and require additional interventions to correct a reversible cause during resuscitation. The evidence for treating these conditions is mostly of low or very low certainty and further studies are needed. Irrespective of the cause, treatments for cardiac arrest are time sensitive and most effective when given early-every minute counts.


Assuntos
Anafilaxia/terapia , Asfixia/terapia , Reanimação Cardiopulmonar/métodos , Parada Cardíaca/terapia , Hipotermia/terapia , Complicações Cardiovasculares na Gravidez/terapia , Embolia Pulmonar/terapia , Ferimentos e Lesões/terapia , Anafilaxia/complicações , Asfixia/complicações , COVID-19/complicações , COVID-19/terapia , Cardioversão Elétrica , Feminino , Parada Cardíaca/etiologia , Humanos , Hipotermia/complicações , Complicações Intraoperatórias/terapia , Parada Cardíaca Extra-Hospitalar/etiologia , Parada Cardíaca Extra-Hospitalar/terapia , Equipamento de Proteção Individual , Complicações Pós-Operatórias/terapia , Guias de Prática Clínica como Assunto , Gravidez , Embolia Pulmonar/complicações , Retorno da Circulação Espontânea , SARS-CoV-2 , Ferimentos e Lesões/complicações
12.
Mitochondrion ; 60: 112-120, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34384933

RESUMO

Cardiac arrest (CA) induces whole-body ischemia resulting in mitochondrial dysfunction. We used isolated mitochondria to examine phospholipid alterations in the brain, heart, kidney, and liver post-CA. Our data shows that ischemia/reperfusion most significantly alters brain mitochondria phospholipids, predominately after resuscitation. Furthermore, the alterations do not appear to be a function of dysregulated importation of phospholipids, but caused by impaired intra-mitochondrial synthesis and/or remodeling of phospholipids. Our data demonstrates only brain mitochondria undergo significant alterations in phospholipids, providing a rationale for the high vulnerability of the brain to ischemia/reperfusion. Furthermore, analyzing this pathophysiologic state provides insight into physiologic mitochondrial phospholipid metabolism.

13.
JAMA Netw Open ; 4(7): e2118801, 2021 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-34323984

RESUMO

Importance: Although racial disparities in acute pain control are well established, the role of patient analgesic preference and the factors associated with these disparities remain unclear. Objective: To characterize racial disparities in opioid prescribing for acute pain after accounting for patient preference and to test the hypothesis that racial disparities may be mitigated by giving clinicians additional information about their patients' treatment preferences and risk of opioid misuse. Design, Setting, and Participants: This study is a secondary analysis of data collected from Life STORRIED (Life Stories for Opioid Risk Reduction in the ED), a multicenter randomized clinical trial conducted between June 2017 and August 2019 in the emergency departments (EDs) of 4 academic medical centers. Participants included 1302 patients aged 18 to 70 years who presented to the ED with ureter colic or musculoskeletal back and/or neck pain. Interventions: The treatment arm was randomized to receive a patient-facing intervention (not examined in this secondary analysis) and a clinician-facing intervention that consisted of a form containing information about each patient's analgesic treatment preference and risk of opioid misuse. Main Outcomes and Measures: Concordance between patient preference for opioid-containing treatment (assessed before ED discharge) and receipt of an opioid prescription at ED discharge. Results: Among 1302 participants in the Life STORRIED clinical trial, 1012 patients had complete demographic and treatment preference data available and were included in this secondary analysis. Of those, 563 patients (55.6%) self-identified as female, with a mean (SD) age of 40.8 (14.1) years. A total of 455 patients (45.0%) identified as White, 384 patients (37.9%) identified as Black, and 173 patients (17.1%) identified as other races. After controlling for demographic characteristics and clinical features, Black patients had lower odds than White patients of receiving a prescription for opioid medication at ED discharge (odds ratio [OR], 0.42; 95% CI, 0.27-0.65). When patients who did and did not prefer opioids were considered separately, Black patients continued to have lower odds of being discharged with a prescription for opioids compared with White patients (among those who preferred opioids: OR, 0.43 [95% CI, 0.24-0.77]; among those who did not prefer opioids: OR, 0.45 [95% CI, 0.23-0.89]). These disparities were not eliminated in the treatment arm, in which clinicians were given additional data about their patients' treatment preferences and risk of opioid misuse. Conclusions and Relevance: In this secondary analysis of data from a randomized clinical trial, Black patients received different acute pain management than White patients after patient preference was accounted for. These disparities remained after clinicians were given additional patient-level data, suggesting that a lack of patient information may not be associated with opioid prescribing disparities. Trial Registration: ClinicalTrials.gov Identifier: NCT03134092.

14.
Crit Care Med ; 2021 Jul 02.
Artigo em Inglês | MEDLINE | ID: mdl-34259447

RESUMO

OBJECTIVES: Cardiac arrest and subsequent resuscitation have been shown to deplete plasma phospholipids. This depletion of phospholipids in circulating plasma may contribute to organ damage postresuscitation. Our aim was to identify the diminishment of essential phospholipids in postresuscitation plasma and develop a novel therapeutic approach of supplementing these depleted phospholipids that are required to prevent organ dysfunction postcardiac arrest, which may lead to improved survival. DESIGN: Clinical case control study followed by translational laboratory study. SETTING: Research institution. PATIENTS/SUBJECTS: Adult cardiac arrest patients and male Sprague-Dawley rats. INTERVENTIONS: Resuscitated rats after 10-minute asphyxial cardiac arrest were randomized to be treated with lysophosphatidylcholine specie or vehicle. MEASUREMENTS AND MAIN RESULTS: We first performed a phospholipid survey on human cardiac arrest and control plasma. Using mass spectrometry analysis followed by multivariable regression analyses, we found that plasma lysophosphatidylcholine levels were an independent discriminator of cardiac arrest. We also found that decreased plasma lysophosphatidylcholine was associated with poor patient outcomes. A similar association was observed in our rat model, with significantly greater depletion of plasma lysophosphatidylcholine with increased cardiac arrest time, suggesting an association of lysophosphatidylcholine levels with injury severity. Using a 10-minute cardiac arrest rat model, we tested supplementation of depleted lysophosphatidylcholine species, lysophosphatidylcholine(18:1), and lysophosphatidylcholine(22:6), which resulted in significantly increased survival compared with control. Furthermore, the survived rats treated with these lysophosphatidylcholine species exhibited significantly improved brain function. However, supplementing lysophosphatidylcholine(18:0), which did not decrease in the plasma after 10-minute cardiac arrest, had no beneficial effect. CONCLUSIONS: Our data suggest that decreased plasma lysophosphatidylcholine is a major contributor to mortality and brain damage postcardiac arrest, and its supplementation may be a novel therapeutic approach.

15.
Front Med (Lausanne) ; 8: 638075, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34150792

RESUMO

This case series reviews four critically ill patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [coronavirus disease 2019 (COVID-19)] suffering from pneumatosis intestinalis (PI) during their hospital admission. All patients received the biological agent tocilizumab (TCZ), an interleukin (IL)-6 antagonist, as an experimental treatment for COVID-19 before developing PI. COVID-19 and TCZ have been independently linked to PI risk, yet the cause of this relationship is unknown and under speculation. PI is a rare condition, defined as the presence of gas in the intestinal wall, and although its pathogenesis is poorly understood, intestinal ischemia is one of its causative agents. Based on COVID-19's association with vasculopathic and ischemic insults, and IL-6's protective role in intestinal epithelial ischemia-reperfusion injury, an adverse synergistic association of COVID-19 and TCZ can be proposed in the setting of PI. To our knowledge, this is the first published, single center, case series of pneumatosis intestinalis in COVID-19 patients who received tocilizumab therapy.

16.
Sci Rep ; 11(1): 12815, 2021 06 17.
Artigo em Inglês | MEDLINE | ID: mdl-34140533

RESUMO

Using a new method for measuring the molecular ratio (R) of inhalation to exhalation, we investigated the effect of high fraction of inspired oxygen (FIO2) on oxygen consumption (VO2), carbon dioxide generation (VCO2), and respiratory quotient (RQ) in mechanically ventilated rats. Twelve rats were equally assigned into two groups by anesthetics: intravenous midazolam/fentanyl vs. inhaled isoflurane. R, VO2, VCO2, and RQ were measured at FIO2 0.3 or 1.0. R error was ± 0.003. R was 1.0099 ± 0.0023 with isoflurane and 1.0074 ± 0.0018 with midazolam/fentanyl. R was 1.0081 ± 0.0017 at an FIO2 of 0.3 and 1.0092 ± 0.0029 at an FIO2 of 1.0. There were no differences in VCO2 among the groups. VO2 increased at FIO2 1.0, which was more notable when midazolam/fentanyl was used (isoflurane-FIO2 0.3: 15.4 ± 1.1; isoflurane-FIO2 1.0: 17.2 ± 1.8; midazolam/fentanyl-FIO2 0.3: 15.4 ± 1.1; midazolam/fentanyl-FIO2 1.0: 21.0 ± 2.2 mL/kg/min at STP). The RQ was lower at FIO2 1.0 than FIO2 0.3 (isoflurane-FIO2 0.3: 0.80 ± 0.07; isoflurane-FIO2 1.0: 0.71 ± 0.05; midazolam/fentanyl-FIO2 0.3: 0.79 ± 0.03; midazolam/fentanyl-FIO2 1.0: 0.59 ± 0.04). R was not affected by either anesthetics or FIO2. Inspired 100% O2 increased VO2 and decreased RQ, which might be more remarkable when midazolam/fentanyl was used.


Assuntos
Expiração/fisiologia , Inalação/fisiologia , Consumo de Oxigênio/fisiologia , Oxigênio/metabolismo , Anestésicos Inalatórios/farmacologia , Animais , Dióxido de Carbono/metabolismo , Expiração/efeitos dos fármacos , Inalação/efeitos dos fármacos , Masculino , Consumo de Oxigênio/efeitos dos fármacos , Pressão , Ratos Sprague-Dawley , Respiração Artificial
17.
Front Med (Lausanne) ; 8: 636651, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34084772

RESUMO

Cardiac arrest (CA) results in global ischemia-reperfusion injury damaging tissues in the whole body. The landscape of therapeutic interventions in resuscitation medicine has evolved from focusing solely on achieving return of circulation to now exploring options to mitigate brain injury and preserve brain function after CA. CA pathology includes mitochondrial damage and endoplasmic reticulum stress response, increased generation of reactive oxygen species, neuroinflammation, and neuronal excitotoxic death. Current non-pharmacologic therapies, such as therapeutic hypothermia and extracorporeal cardiopulmonary resuscitation, have shown benefits in protecting against ischemic brain injury and improving neurological outcomes post-CA, yet their application is difficult to institute ubiquitously. The current preclinical pharmacopeia to address CA and the resulting brain injury utilizes drugs that often target singular pathways and have been difficult to translate from the bench to the clinic. Furthermore, the limited combination therapies that have been attempted have shown mixed effects in conferring neuroprotection and improving survival post-CA. The global scale of CA damage and its resultant brain injury necessitates the future of CA interventions to simultaneously target multiple pathways and alleviate the hemodynamic, mitochondrial, metabolic, oxidative, and inflammatory processes in the brain. This narrative review seeks to highlight the current field of post-CA neuroprotective pharmaceutical therapies, both singular and combination, and discuss the use of an extensive multi-drug cocktail therapy as a novel approach to treat CA-mediated dysregulation of multiple pathways, enhancing survival, and neuroprotection.

18.
Adv Exp Med Biol ; 1269: 39-43, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33966192

RESUMO

Adrenaline is an important pharmacologic treatment during cardiac arrest (CA) for resuscitation. Recent studies suggest that adrenaline increases the likelihood of return of spontaneous circulation (ROSC) but does not contribute to improving neurological outcomes of CA. The mechanisms have not been elucidated yet. A bimodal increase in mean arterial pressure (MAP) is observed after adrenaline injection in rodent CA models [17]. In this study, we focused on alteration of systemic arterial pressure in conjunction with the measurement of cerebral blood oxygenation (CBO) such as oxyhemoglobin (Oxy-Hb), deoxyhemoglobin (Deoxy-Hb), and tissue oxygenation index (TOI) by near-infrared spectroscopy (NIRS). Male Sprague-Dawley rats were used. We attached NIRS between the nasion and the upper cervical spine. Rats underwent 10-minute asphyxia to induce CA. Then, cardiopulmonary resuscitation (CPR) was started, followed by a 20 µg/kg of bolus adrenaline injection at 30 seconds of CPR. This injection accelerated the first increase in MAP, and ROSC was observed with an abrupt increase in CBO. Interestingly, the second increase in MAP, once it exceeded a certain value, was accompanied by paradoxical decreases of Oxy-Hb and TOI, while Deoxy-Hb increased. Based on this finding, we compared Oxy-Hb, Deoxy-Hb, and TOI at the first MAP ≈ 100 mmHg and the second MAP ≈ 100 mmHg. The average of Oxy-Hb and TOI from the 13 animals significantly decreased at the second increase in MAP over 100 mmHg, while Deoxy-Hb significantly increased. NIRS identified a decrease in Oxy-Hb after ROSC. These findings may be a clue to understanding the mechanism of how and why adrenaline alters the neurological outcomes of CA post-resuscitation.


Assuntos
Reanimação Cardiopulmonar , Parada Cardíaca , Animais , Asfixia , Epinefrina , Parada Cardíaca/tratamento farmacológico , Masculino , Oxiemoglobinas , Ratos , Ratos Sprague-Dawley
19.
Adv Exp Med Biol ; 1269: 311-315, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33966235

RESUMO

Clinical investigators have focused on the real-time evaluation of cerebral blood oxygenation (CBO) by near-infrared spectroscopy (NIRS) during cardiopulmonary resuscitation (CPR). A previous study showed that an abrupt increase of oxy-hemoglobin (Hb) level and tissue oxygenation index (TOI) was associated with the timing of return of spontaneous circulation (ROSC). However, it is not clear how TOI alters before and after CPR including a period of cardiac arrest (CA). Therefore, this study aimed to assess CBO with asphyxia CA and its association with CPR to ROSC in rats. Male Sprague-Dawley rats were used. We attached NIRS (NIRO-200NX, Hamamatsu Photonics, Japan) from the nasion to the upper cervical spine in rats. A ten-minute asphyxia was given to induce CA. After CA, mechanical ventilation was restarted, and manual CPR was performed. We examined the mean arterial pressure (MAP), end-tidal carbon dioxide (ETCO2), and Oxy/Deoxy-Hb and TOI. Out of 14 rats, 11 obtained sustained ROSC. After the induction of asphyxia, a rapid drop of TOI was observed, followed by a subsequent increase of Oxy-Hb, Deoxy-Hb, and TOI with CPR. Recent CPR guidelines suggest the use of ETCO2 during CPR since its abrupt increase is a reasonable indicator of ROSC. In this study, abrupt increases in MAP, ETCO2, and TOI were observed at the time of ROSC. TOI can be an alternative to ETCO2 for identifying ROSC after CA, and it also has the capability of monitoring CBO during and after CPR.


Assuntos
Reanimação Cardiopulmonar , Parada Cardíaca , Animais , Asfixia , Parada Cardíaca/terapia , Japão , Masculino , Ratos , Ratos Sprague-Dawley , Espectroscopia de Luz Próxima ao Infravermelho
20.
Endosc Int Open ; 9(5): E701-E705, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33937511

RESUMO

Background and study aims The COVID-19 pandemic has disrupted routine medical care due to uncertainty regarding the risk of viral spread. One major concern for viral transmission to both patients and providers is performing aerosol-generating procedures such as endoscopy. As such, we performed a prospective study to examine the extent of viral contamination present in the local environment before and after endoscopic procedures on COVID-19 positive patients. Materials and methods A total of 82 samples were collected from 23 surfaces in the procedure area of four COVID-positive patients undergoing upper endoscopic procedures. Samples were collected both before and after the procedure. severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA was extracted and quantified using reverse transcription quantitative polymerase chain reaction with primers to detect nucleocapsid RNA, and results reported as the number of viral copies per square centimeter of contaminated surface. Results A total of six positive samples were detected from three of the four patients. The floor beneath the patient bed was the most common site of viral RNA, but RNA was also detected on the ventilator monitor prior to the procedure and the endoscope after the procedure. Conclusions The risk of SARS-CoV-2 transmission associated with upper endoscopy procedures is low based on the low rate of surface contamination. Some surfaces in close proximity to the patient and endoscopist may pose a higher risk for contamination. Patient positioning and oxygen delivery methods may influence the directionality and extent of viral spread. Our results support the use of appropriate personal protection to minimize risk of viral transmission.

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