scholarly journals Pathophysiological and Histopathological Ailments in Asphyxial Cardiac Arrest Induced Ischemic Renal Injury

2021 ◽  
Vol 41 (01) ◽  
pp. 64-70
Author(s):  
Jeong-Hwi Cho

Cardiac arrest (CA) is a sudden interruption in the effective blood flow due to heart failure. The current research aimed to conduct the pathophysiological and histopathological analysis in the kidney in asphyxial cardiac arrest rat model. Cardiac arrest was induced by intravenous injection of vecuronium bromide (2 mg/kg), following stop of mechanical ventilation. Rats were kept on the CA condition for 5 minutes. After that, cardiopulmonary resuscitation (CPR) was done to achieve return of spontaneous circulation (ROSC) following intravenous injection of epinephrine bolus (0.005 mg/kg), sodium bicarbonate (1 mEq/kg) and turn on mechanical ventilation. Then Rats were sacrificed after cardiopulmonary resuscitation (CPR) following asphyxial CA at 6 hrs, 12 hrs, 1 day, 2 days, and 5 days. The intensity of renal injury measured by the serum levels of blood urea nitrogen (BUN), creatinine (Crtn). Moreover, Hematoxylin & eosin, and Periodic Acid Schiff staining in the kidney was done for evaluating the renal histopathological changes. Furthermore, COX-2 immunoreactivity and western analysis were performed in the kidney. Survival rate declined following ROSC compared to the sham group, it showed 80% at 6 hrs and decreased time-dependently to 8% at 5 days. In this study, serum BUN and Crtn levels and renal histopathological scores significantly increased after ROSC in CA. Moreover, COX-2 expression also increased after ROSC in comparison to the sham group with its peak level at 5 days following CA. Renal histological damage score and COX-2 expression were upregulated after ROSC following CA. These results direct that COX-2 takes part in the asphyxial CA-induced ischemic renal injury

2021 ◽  
Vol 7 (17) ◽  
pp. 279-285
Author(s):  
A.A. Avramov ◽  
E.P. Zinina ◽  
D.V. Kudryavtsev ◽  
Y.V. Koroleva ◽  
A.V. Melekhov

Patients with severe lung injury due to COVID-19 are often in need of mechanical ventilation. Due to the predicted length of invasive respiratory support, tracheostomy is commonly indicated to improve patient comfort, to reduce the need for sedation and to allow safer airway care [7] [8] [15]. In this article we report two clinical cases of patients with COVID-19, who suffered cardiac arrest due to problems with tracheostomy canula placement. The first case report is regarding a 74-year-old patient, who was transported to CT from the ICU. Problems first occurred in the elevator, where specialist were forced to switch to bag ventilation, when the oxygen supply ran out. As a result, an episode of desaturation to 80% was registered. Upon arriving in the ICU, the patient was connected to a mechanical ventilator, however ventilation was ineffective: peak pressure was more than 40 cmH2O and the tidal volume was less than 100 ml. Debridement of the trachea was performed, the position of the cannula was secured with no effect. While preparing for oropharyngeal intubation, the patient's saturation dropped to 70%, haemodynamics were unstable (BP 76/40), ECG showed bradycardia of 30 bpm, which quickly turned to asystole. Cardiopulmonary resuscitation was performed and the patient was intubated, mechanical ventilation was effective. The total time of cardiac arrest was around 2 minutes, when ROSC was achieved and sinus rhythm was registered on the ECG. In 6 hours after ROSC signs of acute coronary syndrome were registered, the patient received treatment accordingly. Despite the complications, the patient's condition improved and he was transferred to the therapeutics ward and later discharged home with no signs of neurological impairment. The second case presents a similar clinical situation with an alternate outcome. A 32-year-old patient with COVID-19 was transferred to ICU due to signs of respiratory distress. His condition worsened and the patient was intubated, and soon percutaneous dilatational tracheostomy was performed. On day 9 of treatment in ICU an episode of desaturation to 75% was registered. Debridement of the trachea was not possible due to a block in the cannula. Due to rapid demise in the patient's condition, the cannula was removed and the patient was intubated. After bronchoscopy, re-tracheostomy was performed. During the procedure, it was noted that the standard cannula was displaced at an angle to the posterior wall of the trachea. The cannula was replaced by an armored cannula. In the following hours, hypoxemia was observed, as well as subcutaneous emphysema of the patient's face and upper body. Applying a thoracic X-ray, a left-side pneumothorax was diagnosed, which was urgently drained. In the following days of intensive care the patient's condition gradually improved, mechanical ventilation was effective and signs of respiratory distress were fading. Neurologically the patient was responsive, able to perform simple tasks. Unfortunately, on the 15th day of ICU care the patient's condition worsened: his fever spiked to 39-40,2C, CRP was 149, and CT showed signs of ARDS progression and vasopressors were administered due to hemodynamic instability. An episode of desaturation to 88% was noted. It was assumed that the tracheostomy cannula had been displaced, which was not proven by bronchoscopy. Later that day, while turning the patient to the side, bradycardia was noted on the monitor with progression to asystole. Cardiopulmonary resuscitation was performed for 5 minutes until ROSC. The tracheostomy cannula was then removed, due to inadequate ventilation and the patient was intubated and ventilated through an IT tube. After ROSC the patient's neurological status was closely monitored. Without sedation the patient was unconscious (coma), non-responsive, hyporeflexive with little response to pain stimuli. In two weeks his neurological condition was regarded as a vegetative state (GCS -6).


1996 ◽  
Vol 12 (4) ◽  
pp. 245-248 ◽  
Author(s):  
ROBERT A. BERG ◽  
CHRISTOPHER HENRY ◽  
CHARLES W. OTTO ◽  
ARTHUR B. SANDERS ◽  
KARL B. KERN ◽  
...  

1995 ◽  
Vol 15 (6) ◽  
pp. 1032-1039 ◽  
Author(s):  
Laurence Katz ◽  
Uwe Ebmeyer ◽  
Peter Safar ◽  
Ann Radovsky ◽  
Robert Neumar

An outcome model with asphyxial cardiac arrest in rats has been developed for quantifying brain damage. Twenty-two rats were randomized into three groups. Control group I was normal, was conscious, and had no asphyxia ( n = 6). Sham group II had anesthesia and surgery but no asphyxia ( n = 6). All 12 rats in groups I and II survived to 72 h and were functionally and histologically normal. Arrest group III (the model; n = 10) had light anesthesia and apneic asphyxia of 8 min, which led to cessation of circulation at 3–4 min of apnea, resulting in cardiac arrest (no flow) of 4–5 min. All 10 rats had spontaneous circulation restored by standard external cardiopulmonary resuscitation. Nine rats survived controlled ventilation for 1 h and observation to 72 h, while one rat died before extubation. All nine survivors were conscious at 72 h, with neurologic deficit scores (0% = best; 100% = worst) of 7 ± 69? (2–16%). All brain regions at five coronal levels were examined for ischemic neurons. The prevalence of ischemic neurons in five regions was categorically scored. The average total brain histopathologic damage score in group III ( n = 9) was 2.1 ( p < 0.05 vs. group I or II). A reproducible outcome model of cardiac arrest in rats was documented. It provides a tool for investigating pathophysiological mechanisms of neuronal death caused by a transient global hypoxic–ischemic brain insult.


1985 ◽  
Vol 1 (3) ◽  
pp. 229-236
Author(s):  
G.H. Meuret ◽  
M. Mussler

Rapid and repeated administration of concentrated NaHCO3 solutions during cardiopulmonary resuscitation (CPR) has become routine since the advent of modern resuscitation techniques (1), although it has been pointed out since the early 1960s that acidemia results from prolonged arrest time and that brief arrests may not require NaHCO3 administration (6,8,13). In spite of the widespread use of large amounts of NaHCO3 there is no convincing evidence that the routine use of this drug offers a clear benefit. Only a few studies have been undertaken to ascertain the role of acidosis and acidemia in survival from cardiac arrest, and the possibility of overcorrecting with NaHCO3 in CPR cases (3,4,8,11). Therefore, the intention of this study was: 1) to clarify the role of acidemia in CPR; 2) to investigate the effects of overcorrection of acidemia (leading to metabolic alkalemia; 3) to test the accurate doses of NaHCO3; 4) to examine the optimal sequence of drug administration in CPR, i.e., whether NaHCO3 or epinephrine should be administered as the first drug.During attempts at restoring spontaneous circulation (CPCR Phase II, advanced life support) (12), and during post-CPR prolonged life support (CPCR Phase III) (12), measurements were made in dogs following resuscitation from asphyxial cardiac arrest. The model and methods used have been described in the preceding paper of this Journal. Asphyxial cardiac arrest (mechanical asystole, electromechanical dissociation) was reversed with open-chest CPR and defibrillation as necessary to 20 min max.


2020 ◽  
Vol 94 ◽  
pp. 102761
Author(s):  
Anowarul Islam ◽  
So Eun Kim ◽  
Jae Chol Yoon ◽  
Ali Jawad ◽  
Weishun Tian ◽  
...  

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