Transfusion-related acute lung injury in a COVID-19–positive convalescent plasma recipient: a case report

We present a case of transfusion-related acute lung injury as a complication of convalescent plasma transfusion in a patient who presented with COVID-19–related severe acute respiratory syndrome. Despite treatment with tocilizumab, remdesivir, and intravenous steroids, worsening dyspnea prompted adjunctive treatment with convalescent plasma. Two hours after completion of the plasma transfusion, the patient developed hypoxia-induced cardiac arrest secondary to transfusion-related acute lung injury. This case sheds light on life-threatening transfusion reactions and emphasizes the need to investigate post-transfusion monitoring protocols as well as the possible role of surveillance equipment.

Adverse prognostic factors for rescuing patients with acute myocardial infarction–induced cardiac arrest receiving percutaneous coronary intervention under extracorporeal membrane oxygenation

Background: Acute myocardial infarction–induced cardiac arrest has high mortality rate. Objective: To investigate the risk factors of extracorporeal membrane oxygenation combined with percutaneous coronary intervention in rescuing acute myocardial infarction–induced cardiac arrest. Methods: Forty-three eligible patients were assigned into death and survival groups. Their general clinical data, treatment outcomes, and various indicators 24, 48, and 72 h after extracorporeal membrane oxygenation implantation were compared. The factors affecting clinical outcomes were determined by multivariate logistic regression analysis. A nomogram prediction model was constructed and validated. Results: After removing extracorporeal membrane oxygenation device, 19 patients recovered and 24 died (mortality rate: 55.81%). The two groups had different conventional cardiopulmonary resuscitation duration, number of diseased vessels, distribution of culprit vessel, time from cardiac arrest to extracorporeal membrane oxygenation implantation, length of stay in critical care unit, and mean arterial pressure 24 and 48 h after extracorporeal membrane oxygenation implantation ( p < 0.05). Left anterior descending as the culprit vessel, number of diseased vessels, conventional cardiopulmonary resuscitation duration, time from cardiac arrest to extracorporeal membrane oxygenation implantation, and mean arterial pressure 48 h after extracorporeal membrane oxygenation resuscitation were independent risk factors for death. The predicted mortality rate was 72.6%, and the actual concordance index (C-index) was 0.869. Such indices after internal and external validations were 0.861 and 0.848, respectively, suggesting a good concordance. Conclusion: Left anterior descending as the culprit vessel, number of diseased vessels, conventional cardiopulmonary resuscitation duration, time from cardiac arrest to extracorporeal membrane oxygenation implantation, and mean arterial pressure 48 h after extracorporeal membrane oxygenation resuscitation are independent risk factors for patients with acute myocardial infarction–induced cardiac arrest undergoing extracorporeal membrane oxygenation combined with percutaneous coronary intervention.

Definity, echo contrast, induced cardiac arrest: brief review of the literature

Definity is a contrast media used to enhance the endocardium during echocardiography. Cardiac arrest as an adverse reaction to Definity is still a debate. We are presenting a rare case of a 69-year-old male patient who developed cardiopulmonary arrest immediately after Definity injection during resting echocardiography.

The effect of high-dose intramuscular epinephrine on the recovery of spontaneous circulation in an asphyxia‐induced cardiac arrest rat model

Background Obtaining vascular access can be challenging during resuscitation following cardiac arrest, and it is particularly difficult and time-consuming in paediatric patients. We aimed to compare the efficacy of high-dose intramuscular (IM) versus intravascular (IV) epinephrine administration with regard to the return of spontaneous circulation (ROSC) in an asphyxia-induced cardiac arrest rat model. Methods Forty-five male Sprague-Dawley rats were used for these experiments. Cardiac arrest was induced by asphyxia, and defined as a decline in mean arterial pressure (MAP) to 20 mmHg. After asphyxia-induced cardiac arrest, the rats were randomly allocated into one of 3 groups (control saline group, IV epinephrine group, and IM epinephrine group). After 540 s of cardiac arrest, cardiopulmonary resuscitation was performed, and IV saline (0.01 cc/kg), IV (0.01 mg/kg, 1:100,000) epinephrine or IM (0.05 mg/kg, 1:100,000) epinephrine was administered. ROSC was defined as the achievement of an MAP above 40 mmHg for more than 1 minute. Rates of ROSC, haemodynamics, and arterial blood gas analysis were serially observed. Results The ROSC rate (61.5%) of the IM epinephrine group was less than that in the IV epinephrine group (100%) but was higher than that of the control saline group (15.4%) (log-rank test). There were no differences in MAP between the two groups, but HR in the IM epinephrine group (beta coefficient = 1.02) decreased to a lesser extent than that in the IV epinephrine group with time. Conclusions IM epinephrine induced better ROSC rates compared to the control saline group in asphyxia-induced cardiac arrest, but not compared to IV epinephrine. The IM route of epinephrine administration may be a promising option in an asphyxia-induced cardiac arrest.

Abstract 274: Drugs and Cardiac Arrest: Suffocate the Brain, Spare the Body?

Background: Nearly 70,000 people die of a drug overdose every year. Yet, how drug induced cardiac arrests differ from presumed cardiac etiology cardiac arrests is not well described. In animal models, asphyxial arrests resemble drug induced arrests, demonstrating better hemodynamic profiles yet worse neurologic recovery. Theoretically, this is caused by hypoxemic but preserved perfusion prior to ultimate arrest. But, this has not been studied in humans. We hypothesize that drug induced cardiac arrests will have higher incidence of return of spontaneous circulation (ROSC) in all comers, yet worse neurologic recovery among hospitalized patients. Methods: From a large institutional dataset capturing all patients with out-of-hospital cardiac arrests admitted from 2011 to 2019, we assess the prevalence and outcomes of cardiac arrests, by drug-use status. Patients were excluded if the arrest was trauma induced, occurred in an extended care facility/nursing home, or if treatment was initiated at another medical center. The primary outcome was ROSC in all comers, and the secondary outcome was favorable neurologic function among those surviving to admission. Multivariable logistic regression was used to assess factors associated with differences in outcomes, accounting for traditional cardiac risk factors and arrest characteristics. Results: In total, 436 patients (57±10 years, 31.7% female, 58.5% non-white, 49.3% hypertensive, 28.4% diabetics, and 21.1% preceding coronary disease) were identified, including 94 (21.6%) with drug induced cardiac arrest. Of that total group 101 (23.2%) survived, to admission, 26.6% of the drug induced group and 22.2% of the presumed cardiac cohort, demonstrating no difference in ROSC (P=0.32). Among those that survived to admission, 8% (2/25) of the drug induced group had a favorable neurologic outcome, compared to 29.0% (22/76) of the cardiac induced group (P= 0.03). Following adjustment, the presence of presenting drug induced cardiac arrest remained associated with lower rates of neurologic recovery [OR 7.3 (1.03-51.6) P= 0.04]. There was no difference in survival to discharge. Conclusion: Drug induced cardiac arrest is associated with worse neurologic outcomes than presumed cardiac etiology cardiac arrests.