scholarly journals Higher achieved mean arterial pressure during therapeutic hypothermia is not associated with neurologically intact survival following cardiac arrest

Resuscitation ◽  
2015 ◽  
Vol 88 ◽  
pp. 158-164 ◽  
Author(s):  
Michael N. Young ◽  
Ryan D. Hollenbeck ◽  
Jeremy S. Pollock ◽  
Jennifer L. Giuseffi ◽  
Li Wang ◽  
...  
Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yael Levy ◽  
Alice Hutin ◽  
Nicolas Polge ◽  
fanny lidouren ◽  
Matthias Kohlhauer ◽  
...  

Introduction: Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest but the optimal target to reach for mean arterial pressure (MAP) remains to be determined. Hypothesis: We hypothesized that MAP levels modify cerebral hemodynamics during E-CPR. Accordingly, we tested two MAP targets (65-75 vs 80-90 mmHg) in a porcine model of E-CPR. Methods: Pigs were anesthetized and instrumented for the evaluation of cerebral and systemic hemodynamics. They were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Electric attempts of defibrillation were then delivered until resumption of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min with a standardized volume expansion in both groups. The dose of epinephrine was set to reach either a standard or a high MAP target level (65-75 vs 80-90 mmHg, respectively). Animals were followed during 120 min after ROSC. Results: Six animals were included in both groups. After cardiac arrest, MAP was maintained at the expected level (Figure). During E-CPR, high MAP transiently improved carotid blood flow as compared to standard MAP. This blood flow progressively decreased after ROSC in high vs standard MAP, while intra-cranial pressure increased. Interestingly, this was associated with a significant decrease in cerebral oxygen consumption (26±8 vs 54±6 L O 2 /min/kg at 120 min after ROSC, respectively; p<0.01) (Figure). The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, became positive in high MAP (0.47±0.02) vs standard MAP group (-0.16±0.10), demonstrating altered cerebral autoregulation with high MAP. Conclusion: Increasing MAP above 80 mmHg with epinephrine aggravates cerebral hemodynamics after E-CPR. Figure: Mean arterial pressure (MAP), cerebral blood flow and oxygen consumption (*, p<0.05)


2018 ◽  
Vol 44 (12) ◽  
pp. 2091-2101 ◽  
Author(s):  
Pekka Jakkula ◽  
◽  
Ville Pettilä ◽  
Markus B. Skrifvars ◽  
Johanna Hästbacka ◽  
...  

2019 ◽  
Vol 50 ◽  
pp. 234-241 ◽  
Author(s):  
Johannes Grand ◽  
Christian Hassager ◽  
Matilde Winther-Jensen ◽  
Malin Rundgren ◽  
Hans Friberg ◽  
...  

Author(s):  
Lia M Thomas ◽  
Miguel Benavides ◽  
Pierre Kory ◽  
Samuel Acquah ◽  
Steven Bergmann

Background: Despite advances in out- of- hospital resuscitation practices, the prognosis of most patients after a cardiac arrest remains poor. The long term outcomes of patients successfully resuscitated from cardiac arrest are often complicated by neurological dysfunction. Therapeutic hypothermia has significantly improved neurological outcomes in patients successfully resuscitated from out- of- hospital cardiac arrests. The objective of this study was to look into the neurological outcomes in inpatients after successful cardiopulmonary resuscitation (CPR) in a university hospital setting. Methods: This was a retrospective observational study of 68 adult patients who experienced cardiac or respiratory arrest over an 18 month period at a metropolitan teaching hospital with dedicated, trained code teams. Arrests that occurred in the Emergency Department, Critical Care Units or Operating Rooms were excluded. Results: Of the 68 consecutive patients included in this study, 53% were resuscitated successfully. However, only 12 (18%) survived to discharge from the hospital and only 6 (10%) were discharged with intact neurological status. The initial survival was better in patients who received prompt CPR and in those with less co - morbidities. Pulseless electrical activity (PEA) or asystole were the most common rhythms (47% of the arrests). Most patients who survived and were neurologically intact had PEA (67%). We believe that most PEA arrests were more likely severe hypotension with the inability to palpate a pulse rather than true PEA. The mean time to defibrillation for all patients with an initial shockable rhythm (n=5) was 8.2 minutes. Patients who had an initial shockable rhythm and survived to discharge were shocked within 1 minute (n=2). Conclusion: Despite advances in critical care, survival from inpatient cardiopulmonary arrest to neurologically intact discharge remains poor. Therapeutic hypothermia should be expanded to those resuscitated from in - hospital cardiopulmonary arrest to determine if neurological outcomes would improve.


2021 ◽  
Author(s):  
Yuki Kishihara ◽  
Hideto Yasuda ◽  
Masahiro Kashiura ◽  
Naoshige Harada ◽  
Takashi Moriya

Abstract Background: Sudden cardiac arrest causes numerous deaths worldwide. High-quality chest compressions are important for good neurological recovery. Arterial pressure is considered useful to monitor the quality of chest compressions by the American Heart Association. However, arterial pressure catheter might be inconvenient during resuscitation. Conversely, cerebral regional oxygen saturation (rSO2) during resuscitation may be associated with a good neurological prognosis. Therefore, we aimed to evaluate the correlation between mean arterial pressure and rSO2 during resuscitation to use rSO2 as the indicator of the quality of chest compressions.Methods: This study was a single-centre, prospective, observational study. Patients with out-of-hospital cardiac arrest who were transported to a tertiary care emergency centre between October 2014 and March 2015 in Japan were included. The primary outcome was the regression coefficient between MAP and rSO2. MAP and rSO2 were measured during resuscitation (at hospital arrival [0 min], 3 min, 6 min, 9 min, 12 min, 15 min), and MAP was measured by an arterial catheter inserted into the femoral artery. For analysis, we used the higher value of rSO2 obtained from the left and right forehead of the patient and measured using a near-infrared spectrometer. Regression coefficients were calculated using the generalized estimating equation (GEE) with MAP and SAP as response variables and rSO2 as an explanatory variable, because MAP and rSO2 were repeatedly measured in the same patient. Since the confounding factors between MAP or SAP and rSO2 were not clear clinically or from previous studies, the GEE was analysed using univariate analysis.Results: Thirty-seven patients were analysed. rSO2 and MAP during resuscitation from hospital arrival to 15 min later were expressed as follows (median [interquartile range]): rSO2, 29.5 (24.3–38.8) %, and MAP, 36.5 (26–46) mmHg. The regression coefficient (95% confidence interval) of log-rSO2 and log-MAP was 0.42 (0.03–0.81) (p=0.035).Conclusion: rSO2 and MAP showed a mild but statistically significant association. rSO2 could be used to assess the quality of chest compressions during resuscitation as a non-invasive and simple method.Trial registration: This study was registered in the University hospital Medical Information Network Clinical Trials Registry (UMIN000015479).


Author(s):  
Kiran J. K. Rikhraj ◽  
Michael D. Wood ◽  
Ryan L. Hoiland ◽  
Sharanjit Thiara ◽  
Donald E. G. Griesdale ◽  
...  

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Jing Li ◽  
Xiangdong Zhu ◽  
Matt Oberdier ◽  
Chunpei Lee ◽  
Misha Granado ◽  
...  

Introduction: While effective for out-of-hospital cardiac arrest, therapeutic hypothermia can be difficult to timely implement clinically. No drugs exist for improving neurologically intact survival. We have developed a novel peptide (TAT-PHLPP) that inhibits PH domain and Leucine rich repeat Protein Phosphatases (PHLPP), leading to Akt activation and mimicking of the protective effects of therapeutic hypothermia without the need of physical cooling. Hypothesis: We hypothesize that when administered intravenously during CPR, TAT-PHLPP improves neurologically intact survival. Methods: We conducted parallel studies in mouse and swine models. In C57BL6 mice (n = 72), we induced a 8 or 12-min asystolic cardiac arrest with KCl, followed by initiation of CPR and blinded randomized administration of TAT-PHLPP (7.5 mg/kg) or saline placebo. The primary outcomes were 4-h and 5-day survival, mean arterial blood pressure (MAP) and cerebral blood flow (CBF). We assessed PHLPP-NHERF1 binding and glucose utilization (via pyruvate dehydrogenase (PDH) phosphorylation and ATP generation). In 16 swine, we induced 5 min of VF followed by ACLS with vest CPR and administered two doses of TAT-PHLPP or saline. Survival (24 h) and neurological function were assessed. Plasma biomarkers taurine and glutamate levels in mice were measured and validated in CA patients (n=68) with a shockable rhythm at the time of hospital arrival, 6, 24, 48, and 72 h post-hospital arrival. Results: In mice, compared to saline, TAT-PHLPP significantly improved 4-h and 5-day survival, increased post-ROSC MAP and CBF, inhibited PHLPP-NHERF1 binding, increased p-Akt, decreased p-PDH (increased activity) at 15 min post-ROSC, enhanced ATP generation in both heart and brain, and reduced plasma taurine and glutamate levels. In swine, TAT-PHLPP improved 24 h neurologically intact survival (1/9 in control vs. 6/7 with peptide, p < 0.01). In patients, taurine levels were higher in non-survivors (n=44) than survivors (n=24) at 6 h of post-hospital arrival (65.9 ± 34.8 vs. 45.6 ±23.7, p< 0.001). Conclusions: TAT-PHLPP has high translational potential as a first-of-class biologic treatment to reproduce critical outcomes of therapeutic hypothermia and improve cardiac arrest survival.


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