A comprehensive neuromonitoring approach in a large animal model of cardiac arrest

Background:Anoxic brain injuries represent the main determinant of poor outcome after cardiac arrest(CA).Large animal models have been described to investigate new treatments during CA and post-resuscitation phase,but a detailed model that includes extensive neuromonitoring is lacking.Method:Before an electrically-induced 10-minute CA and resuscitation,46 adult pigs underwent neurosurgery for placement of a multifunctional probe(intracranial pressure or ICP,tissue oxygen tension or PbtO_(2) and cerebral temperature)and a bolt-based technique for the placement and securing of a regional blood flow probe and two sEEG electrodes;two modified cerebral microdialysis(CMD)probes were also inserted in the frontal lobes and accidental misplacement was prevented using a perforated head support.Result:42 animals underwent the CA procedure and 41 achieved the return of spontaneous circulation(ROSC).In 4 cases(8.6%)an adverse event took place during preparation,but only in two cases(4.3%)this was related to the neurosurgery.In 6 animals(13.3%)the minor complications that occurred resolved after probe repositioning.Conclusion:Herein we provide a detailed comprehensive neuromonitoring approach in a large animal model of CA that might help future research.

Code blue applications as an indicator of clinical quality

Objective:To investigate the code blue application at a training and research hospital in Turkey.Methods:The code blue declaration forms and the hospital database with 238 complete records between January 2016 and July 2017 were collected.The form involved individual characteristics,the reason for issuing the code blue call,the unit and block where the code was given,time and location related properties such as working time and arrival duration,properties regarding the intervention process such as its type,duration or result.The 24-hour and 30-day long survival data of the patients to whom cardiopulmonary resuscitation was implemented were obtained from the hospital database,or from their relatives.The influencing factors of arrival duration were analyzed.Results:The median duration of arrival was 2.14(2.00-3.02)min.Code blue applications were performed more frequently in Departments of General Surgery,Internal Medicine,Orthopaedics,and Cardiology Clinics.Half of the code blue calls were due to cardiac arrest;the other half was due to shortness of breath or respiratory distress,syncope,and respiratory arrest.Three-out-of four code blue calls were treated with orotracheal intubation and cardiopulmonary resuscitation,or only orotracheal intubation or only medical treatment;one-fourth of the calls were not intervened.Altogether,72.36%of the code blue calls patients were intervened;69.35%of them were made both orotracheal intubation and cardiopulmonary resuscitation,and 20.5%of them were made only orotracheal intubation and 10.55%of them made only medical treatment.It was found that giving the code blue day or night had no effect on the time to reach the area where the code was given.Similarly,it was found that giving the code blue within daytime or night shift had no effect on the time to reach the area where the code was given.(P>0.05).The survival rates were 39.1%within the first 24 h and 18.1%within the first 30 d.Conclusions:Applications of code blue should be analyzed at regular intervals as clinical quality indicators.Reasons for wrong calls should be determined.The duration of reaching locations where calls are made should also be decreased.

Pump models assessed by transesophageal echocardiography during cardiopulmonary resuscitation

OBJECTIVE: Transesophageal echocardiography was performed during closed-chest cardiopulmonary resuscitation (CPR) in in-hospital cardiac arrest to further explore the hemodynamic mechanism of CPR. METHODS: CPR attempts were performed according to advanced cardiovascular life support guidelines in 6 cases of in-hospital cardiac arrest. Multi-plane transesophageal echocardiography was carried out within 15 min of initiation of CPR. Throughout CPR, the motion of the mitral, tricuspid and aortic valves, the changes in the left ventricular cavity size and the thoracic aortic diameter were observed. Trans-mitral and trans-aortic Doppler files of blood flow were also documented. RESULTS: A closure of the mitral and tricuspid valves with simultaneous opening of the aortic valve occurred exclusively during chest compression, resulting in forward blood flow in the pulmonary and systemic circulation. Peak forward aortic flow at a velocity of 58.8 +/- 11.6 cm/s was recorded during the compression phase. Whereas, a closure of the aortic valve and rapid opening of the atrioventricular valves associated with ventricular filling during relaxation of chest compression was noted in all 6 patients. Peak forward mitral flow at a velocity of 60.6 +/- 20.0 cm/s was recorded during the release phase. Mitral regurgitation during the chest compression period was detected in 5 patients, reflecting a positive ventricular-to-atrial pressure gradient. A reduction in the left ventricular chamber and an increase in the thoracic aortic diameter during the compression phase was found in all patients, indicating that direct cardiac compression contributed to forward blood flow. CONCLUSION: These observations favor the cardiac pump theory as the predominant hemodynamic mechanism of forward blood flow during CPR in human beings.

Effects of subdiaphragmatic cardiac compression on cardiac arrest during liver transplantation

Cardiac arrest during upper abdominal surgery such as liver transplantation is a rare but very severe complication. Traditional external cardiac compression has been the mainstay of basic life support in general circumstances. Subdiaphragmatic cardiac compression （SDCC）, with no incision in the diaphragm, may be a more effective measure. This maneuver can provide more effective and timely cardiac compression via the already open abdomen in surgery and not add extra trauma. This method can provide a quicker and more effective means of circulation support for intraoperative cardiac arrest patients without adding new injuries. Five cases are reported and all the patients had return of spontaneous circulation （ROSC）. This is the first report of the SDCC method.

Protective effects of pinacidil hyperpolarizing cardioplegia on myocardial ischemia reperfusion injury by mitochondrial KATP channels

Background Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels （KATe） were the end effectors of cardio-protection. But whether mitochondrial KATe plays an important role in hyperpolarizing cardioplegia is not apparent. The present study investigated the effect of hyperpolarizing cardioplegia containing pinacidil （a nonselective KATe opener） on ischemia/repeffusion injury in rat hearts, especially the role of mitochondrial KATe in pinacidil hyperpolarizing cardioplegia. Methods Sprague-Dawley rat hearts were Langendorff-perfused for 20 minutes with Krebs-Henseleit buffer at 37℃ before equilibration. Cardiac arrest was then induced in different treatments： there was no arrest and ischemia in the normal group, the control group were arrested by clamping the aorta, depolarizing caidioplegia （St. Thomas solution containing 16 mmol/L KCI） and hyperpolarizing cardioplegia groups used St. Thomas solution containing 0.05 mmol/L pinacidil and 5 mmol/L KCI to induce cardiac arrest in group hyperkalemic and group pinacidil, in group hyperkalemic ＋ 5-hydroxydecanote （5HD） and Pinacidil ＋ 5HD, 5HD （0.1 retool/L） was added to the above two solutions to block mitochondria KATe channels. Global ischemia was then administrated for 40 minutes at 37℃, followed by 30 minutes of reperfusion. At the end of equilibration and reperfusion, hemodynamics, ultrastructure, and mitochondrial function were measured. Results In the control group, ischemia/reperfusion decreased the left ventricular developed pressure, heart rate, coronary flow, mitochondrial membrane potential, impaired mitochondrial respiratory function, increased reactive oxygen species and left ventricular end diastolic pressure. Damage to myocardial ultrastructure was also evident. Both depolarized arrest and especially hyperpolarized cardioplegia significantly reduced these lesions. 5HD partially blocked the beneficial effects of pinacidil cardioplegia but showing no effects on hyperkalemic arrest. Conclusions Pinacidil cardioplegia provides better cardioprotection with preservation of hemodynamics, ultrastructure, and mitochondrial function than traditional cardioplegia. The mitochondria KATe channels may play an important role in the protection mechanism.

Echocardiography integrated ACLS protocol versus con- ventional cardiopulmonary resuscitation in patients with pulseless electrical activity cardiac arrest

Objective： To examine the utility of bedside echocardiography in detecting the reversible causes of pulseless electrical activity （PEA） cardiac arrest and pre dicting the resuscitation outcomes. Methods： In this prospective interventional study, pa tients presenting with PEA cardiac arrest were randomized into two groups. In Group A, ultrasound trained emergency physicians performed echocardiography evaluating cardiac activity, right ventricle dilation, left ventricle function, peri cardial effusion/tamponade and IVC size along with the ad vanced cardiac life support （ACLS） protocol. Patients in Group B solely underwent ACLS protocol without applying echocardiography. The presence or absence of mechanical ventricular activity （MVA） and evidences of PEA reversible causes were recorded. The return of spontaneous circulation （ROSC） and death were evaluated in both groups. Results： One hundred patients with the mean age of （58±6.1） years were enrolled in this study. Fifty patients（Group A） had echocardiography detected in parallel with cardiopulmonary resuscitation （CPR）. Among them, 7 pa tients （14%） had pericardial effusion, 11 （22%） had hypovolemia, and 39 （78%） were revealed the presence of MVA. In the pseudo PEA subgroup （presence of MVA）, 43% had ROSC （positive predictive value） and in the true PEA subgroup with cardiac standstill （absence of MVA）, there was no recorded ROSC （negative predictive value）. Among patients in Group B, no reversible etiology was detected. There was no significant difference in resuscitation results between Groups A and B observed （P=0.52）. Conclusion： Bedside echocardiography can identify some reversible causes of PEA. However, there are no sig nificant changes in survival outcome between the echo group and those with traditional CPR.

Outcome of penetrating cardiac injuries in southern Iran, Shiraz

Objective： Cardiac injuries are one of the most challenging injuries in the field of trauma surgery. Their management often requires immediate surgical intervention, excellent surgical technique and the ability to provide excellent postoperative critical care to patients. The aim of this study was to evaluate the outcome and survival rate of patients with penetrating cardiac injury in southern Iran, Shiraz. Methods： From January 2001 to June 2007, medical records of all patients suffering from penetrating cardiac injuries were reviewed and their outcomes were investigated. The inclusion criterion was the presence of a confirmed penetrating cardiac injury intraoperatively or by autopsy. Patients with blunt cardiac injuries were excluded from the study. Results： The study consisted of 37 patients, including 1 gunshot wound （2.7%）, 35 stab wounds （94.6%） and 1 （2.7%） shotgun wound. The overall survival rate was 76% （28 in 37） and that in stab wound patients was 80%. The collected data of 9 expired patients revealed 11% death on arrival, 67% hypotensive, and 22% normotensive considering physiologic presentation. Paired sample test showed sig- nificant correlation between mortality and electrocardio- graphic changes, amount of retained blood in pericardium, clinical stage and physiologic condition at presentation, as well as associated injury type （gunshot more than stab wound）. Conclusion： Our results show that injury mechanism and initial cardiac rhythm are significant predictors of out- comes in patients with penetrating cardiac injuries. Besides, gunshot injury and exsanguination are the most important predictive variables of mortality.

Variations of Postresuscitation Lung Function after Thrombolysis Therapy in a Cardiac Arrest Porcine Model Caused by Pulmonary Thromboembolism

Background： Study of lung function in survivor from cardiac arrest （CA） caused by pulmonary thromboembolism （PTE） was rare. The aim of this study was to investigate the variations ofpostresuscitation lung function after thrombolysis treatment in a CA porcine model caused by PTE. Methods： After 2 min of untreated CA, pigs of 10-12 weeks with a weight of 30±2 kg （n = 24） were treated with recombinant human tissue plasminogen activator （50 mg）. Cardiopulmonary resuscitation （CPR） and ventilation were initiated after drug administration. Pulmonary function and arterial blood gas parameters were measured at baseline, return of spontaneous circulation （ROSC） immediately, and 1 h, 2 h, 4 h, and 6 h after ROSC. Results： The dynamic lung compliance decreased significantly at ROSC immediately and 1 h after ROSC compared to baseline （21.86 ±2.00 vs. 26.72± 2.20 ml/mmHg and 20.38 ± 1.31 vs. 26.72 ± 2.20 ml/mmHg, respectively; P 〈 0.05; 1 mmHg = 0.133 kPa）. Compared with baseline, airway resistance increased significantly at ROSC immediately and 1 h after ROSC （P 〈 0.05）. Respiratory index also increased after ROSC and showed significant differences among baseline, ROSC immediately, and 2 h after ROSC （P 〈 0.05）. Oxygen delivery decreased at ROSC immediately compared to baseline （P 〈 0.05）. The oxygenation index decreased significantly at any time after ROSC compared to baseline （P 〈 0.05）. Extravascular lung water index and pulmonary vascular permeability index （PVP1） showed significant differences at ROSC immediately compared to baseline and 1 h after ROSC （P 〈 0.05）; PVPI at ROSC inamediately was also different from 6 h after ROSC （P 〈 0.05）. Ventilation/perfusion ratios increased after ROSC （P 〈 0.05）. Histopathology showed fibrin effusion, bleeding in alveoli, and hemagglutinatiun in pulmonary artery. Conclusions： Lung function remains abnormal even after CPR with thrombolysis therapy; it is essential to continue anticoagulation and symptomatic treatment after ROSC.

Study of Cardiac Arrest Caused by Acute Pulmonary Thromboembolism and Thrombolytic Resuscitation in a Porcine Model

Background： The success rate of resuscitation in cardiac arrest （CA） caused by pulmonary thromboembolism （PTE） is low. Furthermore, there are no large animal models that simulate clinical CA. The aim of this study was to establish a porcine CA model caused by PTE and to investigate the pathophysio[ogy of CA and postresuscitation. Methods： This model was induced in castrated male pigs （30 ± 2 kg; n = 21 ） by injecting thrombi （10-15 ml） via the left external jugular vein. Computed tomographic pulmonary angiography （CTPA） was performed at baseline, CA, and return of spontaneous circulation （ROSC）. After CTPA during CA, cardiopulmonary resuscitation （CPR） with thrombolysis （recombinant tissue plasminogen activator 50 mg） was initiated. Hemodynamic, respiratory, and blood gas data were monitored. Cardiac troponins T, cardiac troponin I, creatine kinase-MB, myoglobin, and brain natriuretic peptide （BNP） were measured by enzymeqinked immunosorbent assay. Data were compared between baseline and CA with paired-sample t-test and compared among different time points for survival animals with repeated measures analysis of variance. Results： Seventeen animals achieved CA after emboli injection, while four achieved CA after 5-8 ml more thrombi. Nine animals survived 6 h after CPR. CTPA showed obstruction of the pulmonary arteries. Mean aortic pressure data showed occurrence of CA caused by PTE （Z = -2.803, P = 0.002）. The maximal rate of mean increase of left ventricular pressure （dp/dtmax） was statistically decreased （t = 6,315, P = 0.000, variation coefficient = 0.25）, and end-tidal carbon dioxide partial pressure （PetCO2） decreased to the lowest value （t - 27.240, P = 0.000）. After ROSC （n = 9）, heart rate （HR） and mean right ventricular pressure （MRVP） remained different versus baseline until 2 h after ROSC （HR, P = 0.036; MRVP, P - 0.027）. Myoglobin was statistically increased from CA to 1 h after ROSC （P - 0.036, 0.026, 0,009, respectively）, and BNP was increased from 2 h to 6 h after ROSC （P 0.012, 0.014, 0.039, respectively）. Conclusions： We established a porcine model of CA caused by PTE. The dp/dtmax and PetCO2 may be important for the occurrence of CA, while MRVP may be more important in postresuscitation.