Ventricular Fibrillation Cardiac Arrest Research Articles

Time-Dependent Association Between Agonal Respirations and Cardiopulmonary Resuscitation Hemodynamics in a Porcine Model of Cardiac Arrest

Objective: Agonal respirations (AR) are common in patients with cardiac arrest (CA) and are associated with a higher likelihood of successful return of spontaneous circulation (ROSC). Prior preclinical studies suggest that the favorable effects of AR may be mediated by improved coronary perfusion pressure (CPP) during subsequent cardiopulmonary resuscitation (CPR) efforts, but whether this relationship is influenced by the duration of CA has yet to be studied. Accordingly, we measured CPR hemodynamics in swine following 7 minutes or 10 minutes of untreated ventricular fibrillation (VF) to determine if the frequency of AR is associated with CPP after prolonged CA. Methods: Swine (n=71) were subjected to either 7 minutes (n=50) or 10 minutes (n=21) of electrically-induced VF CA, during which the frequency of AR was recorded before the initiation of CPR with chest compressions (100/minute) and mechanical ventilation (16-20 breaths/minute). CPP was assessed during CPR by calculating the difference between aortic pressure and right atrial pressure during decompression. Animals were retrospectively stratified into two groups (high and low frequency of AR) based on the median number of AR in each cohort (7-minute CA median = 6 AR; 10-minute CA median = 9 AR).>Results: In the 7-minute CA cohort, the high AR group (9.7±2.9 AR; n=28) had a significantly longer time from first to last AR (102±6 vs. 34±6 seconds; p<0.001), shorter time from final AR to CPR initiation (208±8 vs. 280±15 seconds; p<0.001), and higher CPP during CPR (14.4±1.0 vs. 9.3±0.6 mmHg; p<0.001) than the low AR group (2.9±0.4 AR; n=22). In contrast, following 10 minutes of CA, the high AR group (12.0±0.4 AR; n=11) did not have a significantly different CPP during CPR (8.7±1.8 vs. 10.4±1.5 mmHg; p=0.48) when compared to the low AR group (6.2±0.5 AR; n=10). A greater number of defibrillation attempts were required to terminate VF after 10 minutes of CA (3.0±0.6) vs. 7 minutes of CA (1.2±0.1; p<0.001), but this was not impacted by the frequency of AR in either cohort. Conclusion: Consistent with prior studies in swine subjected to 5 minutes of untreated CA, a high frequency of AR during a 7-minute episode of CA was associated with higher CPP upon initiation of CPR. However, the favorable effects of AR frequency on CPP during CPR were no longer apparent when the duration of untreated CA was extended to 10 minutes. These results demonstrate that the beneficial effects of AR on CPR hemodynamics are time-dependent and highlight the importance of early initiation of CPR following CA. Supported by funding from the NIH and US Department of Veteran's Affairs. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Neuronal and myocardial damage in a rat model of ventricular fibrillation cardiac arrest with extracorporeal cardiopulmonary resuscitation

Neuronal and myocardial damage in a rat model of ventricular fibrillation cardiac arrest with extracorporeal cardiopulmonary resuscitation

Abstract 361: Effect of Percutaneous Ventricular Assisted Device on a Recovery of Myocardial Function in Swine Model With Prolonged Cardiac Arrest

Background: Percutaneous ventricular assist device (pLVAD) support and Transient aortic balloon occlusion (AO) can preserve cerebral and cardiac blood flow during cardiopulmonary resuscitation (CPR), but it remains unclear if pLVAD reduces post-cardiac arrest myocardial dysfunction. Hypothesis: pLVAD support immediately after the return of spontaneous circulation (ROSC) improves early recovery of myocardial function following prolonged cardiac arrest. Aims: Evaluate the association between early post-ROSC pLVAD support and recovery of myocardial function in a swine model of prolonged cardiac arrest. Methods: This is a secondary analysis of a subset of animals that achieved ROSC in a study comparing pLVAD, transient AO or both during CPR after prolonged cardiac arrest. pLVAD, aortic occlusion, or both were initiated after 24 minutes of ventricular fibrillation cardiac arrest (8 min no-flow and 16 min mechanical CPR). AO was discontinued post-ROSC, and pLVAD support or standard care were continued. Beginning 60 minutes post-ROSC, pLVAD support was weaned to <1.0 L/min while maintaining a MAP >70 mmHg, and subsequently removed at 4 hours when feasible. The primary outcome was the recovery of cardiac index (CI) and left ventricular ejection fraction (LVEF) at 4 hours post-ROSC. Data are shown as mean (standard error). Results: Seventeen animals achieved ROSC without complication and were included in this analysis (pLVAD group, n = 11 [8 were removed from pLVAD], and standard care group, n = 6). For the primary outcome, the pLVAD group had significantly higher CI of 4.2(0.3) vs. 3.1(0.4) L/min/m2 (p=0.043) and LVEF 60(3) vs. 49(4) % (p=0.029) at 4 hours after ROSC, respectively, when compared with the standard care group. Focusing on the early period within 60 minutes after ROSC when maximum pLVAD flow was maintained, the pLVAD group had significantly higher coronary perfusion pressure (62[4] vs. 47[5] mmHg, p=0.019), lower LV stroke work index (3.9[3.0] vs. 14.9[4.4] cJ/m2, p=0.043), and lower total pulmonary resistance index (13.2[4.8] vs. 21.5[14.4] Wood Unit, p=0.001). Conclusion: These results suggest that early pLVAD support after ROSC is associated with better recovery myocardial function compared to standard care after prolonged cardiac arrest.

Abstract 19084: The Deadly Squeeze - Coronary Vasospasm Complicated by Myocardial Infarction and Cardiac Arrest

Introduction: Acute coronary syndrome (ACS) typically results from atherosclerotic plaque rupture. However, about 6% of ST elevation Myocardial Infarction (STEMI) patients have no obstructive disease. We present a case of STEMI, diagnosed with coronary vasospasm. Hypothesis: Methods: A 54-year-old female with alcohol abuse, smoking and uncontrolled hypertension presented after an out of hospital ventricular fibrillation cardiac arrest. EKG showed anterolateral ST elevation (STE). Left heart catheterization (LHC) showed moderate to severe multi-vessel disease without a definitive culprit lesion. STE resolved. Heart team approach for revascularization was contemplated. Echocardiogram showed systolic dysfunction with ejection fraction (EF) of 25%. Patient had another cardiac arrest and EKG showed recurrent anterolateral STE. Repeat LHC showed severe vasospasm of Left anterior descending (LAD) artery and diagonal branch, which improved with intracoronary (IC) nitroglycerin. Vasospasm was attributed to smoking and catecholamine excess from alcohol withdrawal. She was started on intravenous nitroglycerin and amlodipine. Her hospital course was complicated by high degree AV block requiring temporary pacer. She was eventually extubated with good neurological recovery and recovered systolic function (EF 60%). She was counselled on smoking and alcohol cessation and discharged home on isosorbide dinitrate and Amlodipine with planned surgical revascularization. Results: Coronary vasospasm (CVS) can occur both in normal and diseased coronaries. Risk factors include smoking, alcohol use and withdrawal, cocaine, mental stress, etc. Vasospasm may present as Prinzmetal’s angina, myocardial infarction, AV block, or fatal arrhythmias. IC nitroglycerine during LHC aids in diagnosis of CVS in setting of ACS. IVUS (Intravascular ultrasound) may help diagnose presence or absence of concomitant atherosclerotic disease. Provocative testing with IC ergonovine and acetylcholine may be considered in non-ACS setting. Conclusions: This case emphasizes the need to have a high index of suspicion for vasospasm to prevent associated complications and establish an accurate diagnosis and guide proper management of this potentially fatal disease.

Effect of no-flow period on the vasopressor effect of initial epinephrine administration in cardiac arrest

ObjectivesWhether a longer no-flow (NF) interval affects the magnitude of response to epinephrine in the resuscitation has not been well studied. Therefore, this study aimed to evaluate the effect of NF interval on the vasopressor effect of initial epinephrine administration in a porcine model. MethodsWe enrolled 20 pigs from two randomized porcine experimental studies using a ventricular fibrillation (VF) cardiac arrest model. The first experiment subjects were resuscitated after 4 min of NF (Short NF group), followed by three cycles (6 min) of chest compression using a mechanical cardiopulmonary resuscitation device before epinephrine administration. Second experiment subjects received 6 min of NF (Long NF group), two cycles (4 min) of chest compressions, and administration of epinephrine. Defibrillation for VF was delivered 8 and 10 min after VF induction in the Short NF and Long NF groups, respectively. The mean arterial pressure (MAP) and cerebral perfusion pressure (CePP) in the 2-min resuscitation period after epinephrine administration were compared between the study groups using the Wilcoxon rank-sum test. The mean differences in the parameters between phases were also compared. ResultsSeven pigs in the Short NF group and 13 pigs in the Long NF group were included in the analysis. All 2-min resuscitation phases from 6 to 16 min after VF induction were compared between the study groups. The Short NF group showed higher MAP and CePP in all phases (p < 0.01). Change of mean MAP after the epinephrine administration was significantly different between the study groups: mean difference (95% confidence interval) of 16.6 (15.8–17.4) mmHg in the Short NF group and 4.2 (3.9–4.5) mmHg in the Long NF group. ConclusionIn the porcine VF cardiac arrest model, 6 min of NF before resuscitation may affect the vasopressor effect of the initial epinephrine administered compared to 4 min of NF. A short NF may play a role in maximizing the effect of epinephrine in advanced cardiovascular life support.

A ventricular fibrillation cardiac arrest model with extracorporeal cardiopulmonary resuscitation in rats: 8 minutes arrest time leads to increased myocardial damage but does not increase neuronal damage compared to 6 minutes.

Extracorporeal cardiopulmonary resuscitation (ECPR) is an emerging strategy in highly selected patients with refractory cardiac arrest (CA). Animal models can help to identify new therapeutic strategies to improve neurological outcome and cardiac function after global ischemia in CA. Aim of the study was to establish a reproducible ECPR rat model of ventricular fibrillation CA (VFCA) that leads to consistent neuronal damage with acceptable long-term survival rates, which can be used for future research. Male Sprague Dawley rats were resuscitated with ECPR from 6 min (n = 15) and 8 min (n = 16) VFCA. Animals surviving for 14 days after return of spontaneous resuscitation (ROSC) were compared with sham operated animals (n = 10); neurological outcome was assessed daily until day 14. In the hippocampal cornu ammonis 1 region viable neurons were counted. Microglia and astrocyte reaction was assessed by Iba1 and GFAP immunohistochemistry, and collagen fibers in the myocardium were detected in Azan staining. QuPath was applied for quantification. Of the 15 rats included in the 6 min CA group, all achieved ROSC (100%) and 10 (67%) survived to 14 days; in the 8 min CA group, 15 (94%) achieved ROSC and 5 (31%) reached the endpoint. All sham animals (n = 10) survived 2 weeks. The quantity of viable neurons was significantly decreased, while the area displaying Iba1 and GFAP positive pixels was significantly increased in the hippocampus across both groups that experienced CA. Interestingly, there was no difference between the two CA groups regarding these changes. The myocardium in the 8 min CA group exhibited significantly more collagen fibers compared to the sham animals, without differences between 6- and 8-min CA groups. However, this significant increase was not observed in the 6 min CA group. Our findings indicate a uniform occurrence of neuronal damage in the hippocampus across both CA groups. However, there was a decrease in survival following an 8-min CA. Consequently, a 6-min duration of CA resulted in predictable neurological damage without significant cardiac damage and ensured adequate survival rates up to 14 days. This appears to offer a reliable model for investigating neuroprotective therapies.

Effect of percutaneous ventricular assisted device on post-cardiac arrest myocardial dysfunction in swine model with prolonged cardiac arrest

BackgroundIt remains unclear if percutaneous left ventricular assist device (pLVAD) reduces post-cardiac arrest myocardial dysfunction. MethodsThis is a prespecified analysis of a subset of swine that achieved return of spontaneous circulation (ROSC) in a study comparing pLVAD, transient aortic occlusion (AO), or both during cardiopulmonary resuscitation (CPR). Devices were initiated after 24 minutes of ventricular fibrillation cardiac arrest (8 min no-flow and 16 min mechanical CPR). AO was discontinued post-ROSC, and pLVAD support or standard care were continued. Beginning 60 minutes post-ROSC, pLVAD support was weaned to < 1.0 L/min and subsequently removed at 240 minutes. The primary outcome was cardiac index (CI), stroke volume index (SVI), and left ventricular ejection fraction (LVEF) at 240 minutes post-ROSC. Data are shown as mean (standard error). ResultsSeventeen swine achieved ROSC without complication and were included in this analysis (pLVAD group, n = 11 and standard care group, n = 6). For the primary outcomes, the pLVAD group had significantly higher CI of 4.2(0.3) vs. 3.1(0.4) L/min/m2 (p = 0.043) and LVEF 60(3) vs. 49(4) % (p = 0.029) at 240 minutes after ROSC when compared with the standard care group, while SVI was not statistically significantly different (32[3] vs. 23[4] mL/min/m2, p = 0.054). During the first 60 minutes post-ROSC, the pLVAD group had significantly higher coronary perfusion pressure, lower LV stroke work index, and total pulmonary resistance index. ConclusionThese results suggest that early pLVAD support after ROSC is associated with better recovery myocardial function compared to standard care after prolonged cardiac arrest.

Impact of the hybrid emergency department on resuscitation strategies and outcomes in ventricular fibrillation

BackgroundThe Hybrid emergency room (ER) is a novel resuscitation room that includes a whole-body computed tomography scanner and angiography system, which enables physicians to seamlessly conduct resuscitation, diagnosis and therapeutic interventions without patient transfer. This study aimed to assess the impact of the Hybrid ER on mortality in patients with ventricular fibrillation cardiac arrest. MethodsThis was a retrospective cohort study conducted in a tertiary hospital in Japan. We consecutively included adult cardiac arrest patients who were transferred to the emergency departments from January 2007 to May 2020, and were confirmed to be in ventricular fibrillation within 10 min from patient arrival. The study population was divided into two groups: the conventional group (from January 2007 to July 2011) and the Hybrid ER group (from August 2011 to May 2020). The primary endpoint of this study was defined as all-cause in-hospital death. Secondary endpoints included the frequency of extracorporeal cardiopulmonary resuscitation (ECPR) and percutaneous coronary intervention (PCI), and door-to-balloon time and door-to-ECPR time. ResultsWe included 115 patients in the conventional group and 185 patients in the Hybrid ER group. In-hospital mortality was significantly decreased in the Hybrid ER group (adjusted hazard ratio, 0.79; 95% confidence interval 0.64, 0.97; p = 0.026). Door-to-ECPR time was significantly shorter in the Hybrid ER group (p < 0.001, Gehan-Breslow-Wilcoxon test), as was door-to-balloon time in this group (p = 0.004, Gehan-Breslow-Wilcoxon test). In interrupted time-series analyses, it was visually recognized that the ratio of patients who received ECPR and PCI increased, and door-to-ECPR time and door-to-balloon time were shortened from 2011 to 2012 (before and after installation of the Hybrid ER). ConclusionInstallation of the Hybrid ER was associated with a reduced time to ECPR and PCI and with a possible improvement in survival in patients with ventricular fibrillation cardiac arrest.

Age, sex, and survival following ventricular fibrillation cardiac arrest: A mechanistic evaluation of the ECG waveform

BackgroundStudies of outcome differences by sex in out-of-hospital cardiac arrest (OHCA) have produced mixed results that may depend on age, a potential surrogate for menopausal status. ObjectiveWe used quantitative measures of ventricular fibrillation (VF) waveforms – indicators of the myocardium’s physiology – to assess whether survival differences according to sex and age group may be mediated via a biologic mechanism. MethodsWe conducted a cohort study of VF-OHCA in a metropolitan EMS system. We used multivariable logistic regression to assess the association of survival to hospital discharge with sex and age group (<55, ≥55 years). We determined the proportion of outcome difference mediated by VF waveform measures: VitalityScore and amplitude spectrum area (AMSA). ResultsAmong 1526 VF-OHCA patients, the average age was 62 years, and 29% were female. Overall, younger women were more likely to survive than younger men (survival 67% vs 54%, p = 0.02), while survival among older women and older men did not differ (40% vs 44%, p = 0.3). Adjusting for Utstein characteristics, women <55 compared to men <55 had greater odds of survival to hospital discharge (OR = 1.93, 95% CI 1.23–3.09), an association not observed between the ≥55 groups. Waveform measures were more favorable among women and mediated some of the beneficial association between female sex and survival among those <55 years: 47% for VitalityScore and 25% for AMSA. ConclusionsWomen <55 years were more likely to survive than men <55 years following VF-OHCA. The biologic mechanism represented by VF waveform mediated some, though not all, of the outcome difference.

Differences in Cerebral Oxygenation in Cardiogenic and Respiratory Cardiac Arrest Before, During, and After Cardiopulmonary Resuscitation.

We compared the changes in cerebral oxygen saturation (ScO2) levels during cardiac arrest (CA) events using porcine models of ventricular fibrillation CA (VF-CA) and asphyxial CA (A-CA). Twenty female pigs were randomly divided into VF-CA and A-CA groups. We initiated cardiopulmonary resuscitation (CPR) 4 min after CA and measured the cerebral tissue oxygenation index (TOI) using near-infrared spectroscopy (NIRS) before, during, and after CPR. In both groups, the TOI was the lowest at 3-4 min after pre-CPR phase initiation (VF-CA group: 3.4 min [2.8-3.9]; A-CA group: 3.2 min [2.9-4.6]; p = 0.386). The increase in TOI differed between the groups in the CPR phase (p < 0.001); it increased more rapidly in the VF-CA group (16.6 [5.5-32.6] vs. 1.1 [0.6-3.3] %/min; p < 0.001). Seven pigs surviving for 60 min after the return of spontaneous circulation in the VF-CA group recovered limb movement, whereas only one in the A-CA group (p = 0.023) achieved movement recovery. The increase in the TOI did not differ significantly between the groups in the post-CPR phase (p = 0.341). Therefore, it is better to monitor ScO2 concomitantly with CPR initiation using NIRS to assess the responsiveness to CPR in clinical settings.

Esmolol, vector change, and dose-capped epinephrine for prehospital ventricular fibrillation or pulseless ventricular tachycardia

BackgroundRefractory ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT) cardiac arrest describes a subset of patients who do not respond to standard Advanced Cardiac Life Support (ACLS) interventions and are associated with poor outcomes. Esmolol administration and vector change defibrillation have shown promise in improving outcomes in these patients, however evidence is limited. ObjectivesThis study compares clinical outcomes between patients with prehospital refractory VF/pVT who received an Emergency Medical Service (EMS) bundle, comprised of esmolol administration, vector change defibrillation, and dose-capped epinephrine at 3 mg, to patients who received standard ACLS interventions. MethodsThis multicenter, retrospective, cohort study evaluated medical records between October 18, 2017 and March 15, 2022. Patients were enrolled if they experienced a prehospital cardiac arrest with the rhythm VF or pVT, had received at least three standard defibrillations, at least 3 mg of epinephrine, and 300 mg of amiodarone. Patients who received the EMS bundle after its implementation were compared to patients who received standard ACLS interventions prior to its implementation. The primary outcome was sustained return of spontaneous circulation (ROSC), defined as ROSC lasting 20 min without recurrence of cardiac arrest. Secondary outcomes included the incidence of any ROSC, survival to hospital arrival, survival at hospital discharge, and neurologically intact survival at hospital discharge. ResultsEighty-three patients were included in the study. Thirty-six were included in the pre-EMS bundle group and 47 patients were included in the post-EMS bundle group. Patients in the pre-EMS bundle group achieved significantly higher rates of sustained ROSC (58.3% vs 17%, p < 0.001), any ROSC (66.7% vs 19.1%, p < 0.001), and survival to hospital arrival (55.6% vs 17%, p < 0.001). The rates of survival to hospital discharge (16.7% vs 6.4%, p = 0.17) and neurologically intact survival at hospital discharge (5.9% vs 4.3%, p = 1.00) were not significantly different between groups. ConclusionsPatients who received the EMS bundle achieved sustained ROSC significantly less often and were less likely to have pulses at hospital arrival. The incidence of neurologically intact survival was low and similar between groups.

Abstract 230: Spinal Cord Injury In A 14 Days Survival Rat Model Of 6 And 8 Min Of Ventricular Fibrillation Cardiac Arrest, Resuscitated With Conventional Chest Compression

Introduction: Impact of global ischemia and reperfusion on brain in resuscitation animal models is well investigated. Investigations on vulnerability of spinal cord in such models are rarely reported. We investigated the spinal cord in a cardiopulmonary resuscitation ventricular fibrillation cardiac arrest (VFCA) rat model and hypothesized that an untreated CA of 6 and 8 min will lead to histological damage and dysfunction in the resuscitated animal′s spinal cord, depending on CA duration. Methods: Adult male Sprague-Dawley rats (350-450 g) were subjected to 6 (n=8) or 8 min (n=14) of VFCA and resuscitated with conventional chest compressions with a thumper device, mechanical ventilation and drugs (epinephrine, bicarbonate, heparin). After defibrillation and ROSC, rats survived for 14 days. The spinal cord was removed from the spine after fixation in formalin and embedded in paraffin. Transverse sections of cervical, thoracic and lumbar spinal cord were stained with hematoxylin and eosin (HE). Immunohistochemistry was performed with antibodies against GFAP for astrocytes and Iba1 for microglia. Sections were evaluated by a pathologist blinded to treatment regimens, and compared to sham animals (n=5). Results: Resuscitated animals showed high mortality; after 6 min CA four animals and after 8 min CA eleven animals died before endpoint. Surviving animals showed focal bilateral symmetrical loss of neurons and distinct gliosis in the gray matter of the thoracic spinal cord level with the central canal. Similar lesions were detected in other segments of the spinal cord, but were located predominantly in the ventral horn of the spinal cord. These lesions were accompanied by dilated myelin sheaths in the white matter. Immunohistochemistry showed activation of astrocytes and microglia in the damaged regions. There were no differences detectable between animals subjected to 6 or 8 min VFCA. Sham animals showed no lesions in the spinal cord. Conclusions: We found consistent histological damage in the spinal cords of rats resuscitated after 6 and 8 min untreated VFCA with CPR after 14 days survival but without clinical symptoms in these animals. However, similar lesions might be cause of paralysis and urinary retention found in animals that died before endpoint.

Abstract 11350: Arrhythmogenic Mitral Valve Prolaspe and Mitral Annular Disjunction

Background: Mitral valve prolapse (MVP) affects about 2-3% of the general population. A small proportion of persons may have arrhythmic symptoms, leading to ventricular arrhythmias and sudden cardiac death (SCD). Mitral annular disjunction is a recently described entity that may be present with MVP or independently. Case: A 55-year-old male patient presented to the hospital with cardiac arrest. He has a history of percutaneous coronary intervention with stenting to left anterior descending (LAD) and right coronary artery (RCA) in 2015. He had ventricular fibrillation (VF) and subsequently arrested and underwent resuscitation. Electrocardiogram (EKG) showed sinus rhythm with prolonged QTc 487msec with no ischemia; echocardiography showed mitral annular disjunction, severe left ventricular global hypokinesis with ejection fraction of 10%. Left heart catheterization revealed nonobstructive moderate coronary artery disease. Right heart catheterization showed a severely reduced cardiac index of 2.1, and he was placed on mechanical support (Impella) for cardiogenic shock. On day 5, repeat echocardiography revealed left ventricular ejection fraction of 60%. Subsequent cardiac magnetic resonance (CMR) showed no evidence of infiltrative diseases but revealed an inferolateral wall scar from previous myocardial infarction and MVP with MAD. An implantable cardiac defibrillator was placed for secondary prevention of SCD. Discussion: The potential etiology of our patient's ventricular fibrillation cardiac arrest may include a scar from previous myocardial infarction or arrhythmogenic MVP with MAD. Myocardial fibrosis arising from MAD may be an origin of ectopic activity and arrhythmia. EKG, echocardiographic, and cardiac magnetic resonance imaging (CMR) are essential in diagnosing arrhythmic MVP and MAD. Young patients with premature ventricular contractions without clear etiology should be evaluated for MAD, and incidental findings of MAD should warrant further investigations, given its arrhythmogenic potential. Conclusion: MVP with MAD is associated with life-threatening arrhythmias. Further studies are required to explore treatment options to reduce the incidence of malignant VAs and SCDs in patients with MVP.

Abstract 13169: Cardiac Arrest and Severe Arterial Vasospasm in a 37-Year-Old Woman With Recent Covid Infection

CASE: A 37-year-old woman with history of smoking, hypertension and mild COVID-19 diagnosed 40 days prior with intermittent chest pain since then presented to the emergency department (ED) via EMS for an out-of-hospital ventricular fibrillation cardiac arrest. She was resuscitated at home with a downtime of 15 minutes. Her initial ED EKG was normal and she was admitted to the cardiac ICU. Shortly after admission she developed a junctional rhythm with ST elevation in lead II followed by polymorphic ventricular tachycardia which degenerated into ventricular defibrillation. She received 3 shocks with subsequent resuscitation. She was started on an amiodarone drip and underwent coronary angiography. With right femoral artery engagement she was noted to have severe vasospasm. An initial angiogram of the left coronary system showed mild coronary disease, subsequent injection showed diffuse vasospasm in the entire left coronary system. Telemetry showed diffuse ST elevations and QT widening with injections followed by ventricular fibrillation treated with 8 counter-shocks and the addition of lidocaine. An intra-aortic balloon pump was placed prior to transfer back to the ICU. She was initially treated with nicardipine and transitioned to amlodipine for treatment of vasospasm. Rheumatologic work-up was unremarkable and she underwent placement of an ICD for secondary prevention. A Coronary CT was performed in follow-up showing only minimal luminal irregularities with no RCA disease. DISCUSSION: COVID-19 has been linked to many cardiovascular abnormalities including diffuse vasospasm with acute infection. This is the first case describing diffuse vasospasm in a person who is in the post-COVID period which is defined as greater than 4 weeks after diagnosis. This case provides information on severe arterial vasospasm seen in the time period after acute COVID infection indicating that follow up after COVID for any cardiovascular abnormalities is needed.

Abstract 231: Volume And Direction Of Carotid Blood Flow During Cardiopulmonary Resuscitation In A Porcine Model Of Ventricular Fibrillation

Introduction: Hemodynamics during cardiopulmonary resuscitation (CPR) is not well understood. We aimed to quantitatively evaluate the volume and direction of carotid blood flow (CBF) during CPR in a porcine model of ventricular fibrillation (VF) cardiac arrest. Methods: Nineteen male domestic pigs were intubated and ventilated mechanically. Following baseline measurements, VF was electrically induced. CBF was measured continuously using a flow probe positioned around the common carotid arteries. After 0 or 5 min no-flow time of untreated VF, CPR was initiated, involving chest compressions and ventilation with oxygen. CPR was continued for 25 min, with mechanical (L1, L2, and L3) and manual (M1 and M2) CPR alternated at 5 min intervals. A Friedman test was used to compare the groups in each phase. Post hoc analysis was performed using a Wilcoxon signed-rank test (Bonferroni corrected). Results: CBF was calculated as the average of each phase. The net flow was calculated through subtracting the retrograde flow from the anterograde flow. Average net flow (median, interquartile range [IQR], mL/min) during CPR was 58.1 (24.0-111.3), 19.8 (8.4-24.9), 21.2 (9.5-37.9), 15.4 (8.4-24.9), and 16.4 (10.3-30.1) in phases L1, M1, L2, M2, and L3, respectively ( p &lt; 0.001, L1 vs. M1). The ratio (median, IQR, %) of retrograde to anterograde flow was 41.3 (16.7-58.7), 48.6 (33.1-60.4), 42.2 (36.5-76.4), 49.1 (39.4-68.5), and 50.0 (38.0-79.0) in phases L1, M1, L2, M2, and L3, respectively ( p = 0.299). Conclusions: In this VF cardiac arrest model, the net flow of the carotid artery during CPR decreased with time. Both mechanical and manual CPR produced substantial retrograde flow, although the ratio of retrograde to anterograde flow did not change.

Abstract 196: Association Between Continuous Carotid Blow Flow And Continuous Cerebral Perfusion Indexes Assessment By NIRS In A Porcine Model Of Ventricular Fibrillation During CPR

[Background]: Maintenance of cerebral blood flow during cardiopulmonary resuscitation (CPR) is a critical factor affecting the neurological outcome of patients after cardiac arrest. However, dynamic indicator of cerebral blood flow during CPR is not established. Near infrared spectroscopy (NIRS) is a non-invasive technique capable of detecting changes in cerebral blood volume continuously. The aim of this study is to compare cerebral perfusion during CPR obtained by continuous measure of carotid blow flow (CBF) using flow sensor with continuous cerebral perfusion indices (CPI) assessment by NIRS in a porcine model of ventricular fibrillation (VF) cardiac arrest. [Methods]: CBF during CPR were measured in 21 swine (25± 3 kg) using extra-vascular flow probes positioned around the common carotid arteries. The optodes of the NIRS were attached to the skull bone. Following baseline measurements, VF was electrically induced. After the interval of untreated VF, CPR was continued for 25 min, during which mechanical and manual CPR was alternated at every 5 min intervals. CBF and CPI were measured continuously during CPR. The mean volume of CBF and CPI was calculated average 10 beats in each phase. Correlations between CBF volume and CPI were analyzed by Spearman's rank correlation. [Results]: The followability of CBF and CPI during CPR was good. The Spearman's rank correlation coefficient between CBF volume and CPI was different by sections and it was suggested that the CBF volume was too small to assess the correlation in many sections. If the sections with CBF volume&gt;0.4 ml were extracted and reanalyzed, the rate of sections correlated between CBF volume and CPI were increased (Spearman’s correlation coefficient≧0.4 was 41.3%, Spearman’s correlation coefficient≧0.7 was 17.5%).(Table) [Conclusions]: It was suggested that CPI by NIRS can reflect the CBF during CPR in the sections where enough CBF is.

Abstract 161: Impact Of Leukocyte Filtration And Leukocyte Modulation On Myocardial Injury After Prolonged Cardiac Arrest Treated With Extracorporeal Cardiopulmonary Resuscitation In A Swine Model

Background: Post-arrest myocardial dysfunction is one of the major causes of rearrest within early period after return of spontaneous circulation (ROSC). Multiple interacting processes including leukocyte-mediated injury is suspected to contribute to deterioration of cardiac function after cardiac arrest. Unlike the standard leukocyte filter (LF), the leukocyte modulation (L-MOD) device is expected to alter the natural inflammatory process by preferentially binding and inactivating the activated leukocytes. We tested the hypothesis that either a standard LF system or a L-MOD device will decrease myocardial injury during extracorporeal cardiopulmonary resuscitation (ECPR). Methods: Total 34 swine (45.5±2.5 kg, male=18, female=16) underwent 8 minutes of untreated ventricular fibrillation cardiac arrest followed by mechanical CPR for 30 minutes. Immediately followed by 8 hours of ECPR with randomly assigned leukocyte treatment protocol; ECPR with standard care (n=10), LF (n=12), and L-MOD (n=12). Left ventricular ejection fraction (LVEF) was evaluated hourly by transthoracic echocardiography. At the end of the study, the heart was removed, fixed and embedded in paraffin. 5- μm sections off the left and right ventricular (RV) free wall were H &amp; E stained for analysis. Five views each of LV and RV under 20хobjective lens were randomly selected with Leica LAS X software. Myofiber degeneration and hemorrhage were graded as 0 (absence) to 3 (severe). Grade was average of 5 views. Results: The mean LVEF at baseline was 65±6%. There were no significantly difference in rate of achieving ROSC (70% vs. 75% vs. 58.3%, p=0.671) and LVEF at 8 hours after initiating ECPR (35±27% vs. 36±31% vs. 28±30%, p=0.776) between the group with control, LF, and LMOD respectively. There were no significant difference in myofiber degeneration grade (LV, 1.5±0.5 vs. 1.1±0.6 vs. 1.4±0.4, p=0.334; and RV, 1.6±0.6 vs. 1.8±0.7 vs. 1.5±0.6, p=0.525) and hemorrhage grade (LV, 0.0±0.1 vs. 0.0±0.1 vs. 0.0±0.1, p=0.841; and RV, 0.0±0.0 vs. 0.0±0.0 vs. 0.0±0.0) between control, LF, and L-MOD groups. Discussion: In swine model with prolonged cardiac arrest treated with ECPR, a standard LF system and a L-MOD device did not decrease early myocardial injury.

Abstract 217: Association Of Ventricular Fibrillation Instantaneous Amplitude At Time Of Defibrillation With Resuscitation Outcome

Introduction: Quantitative measures of the ventricular fibrillation (VF) ECG waveform predict defibrillation outcomes. A prior study observed that greater Instantaneous Amplitude (IA) of the VF ECG, measured at the instant of defibrillation (Figure), predicted better outcome independent of other VF measures. If true, resuscitation might be improved by synchronizing shock to ECG amplitude. We sought to determine whether IA was an independent predictor of shock-specific outcome using a larger independent dataset. Methods: We investigated adult out-of-hospital VF cardiac arrest cases in a metropolitan EMS system treated with a Philips MRx defibrillator. For each shock, we computed the IA as the absolute value of the ECG at the time of shock delivery. We also computed the amplitude spectrum area (AMSA), a well-characterized waveform measure, from the 3-second CPR-free period preceding the shock. Study outcome was return of spontaneous circulation (ROSC) after each shock. We used Wilcoxon test to evaluate the unadjusted relationship between IA and shock-specific ROSC, and a generalized linear mixed-effect (GLME) model to assess whether IA was associated with shock-specific ROSC independent of AMSA. Results: We included 1516 shocks from 567 patients, with a median (IQR) of 2 (1-3) shocks per patient and shock-specific ROSC rate of 22% (337/1516). IA was correlated with AMSA; Pearson’s R = 0.43. Median (IQR) IA was greater for shocks that resulted in ROSC, with IA of 0.14 (0.05-0.25) mV vs 0.09 (0.04-0.18) mV, (p&lt;0.001). However, when both IA and AMSA were included in a GLME model, AMSA was significantly associated with ROSC (OR 2.09, 95% CI 1.74-2.50 for an IQR change in AMSA) but IA was not (OR 1.04, 95% CI 0.92-1.18 for an IQR change in IA). Conclusions: IA did not independently predict ROSC after controlling for AMSA. Thus, IA is likely a surrogate for other waveform measures, limiting its usefulness to guide instantaneous defibrillation timing as a means to improve outcome.

Abstract 305: Effect Of Initial Epinephrine Administration Time On Cerebral Perfusion In A Porcine Experimental Model Of Cardiac Arrest

Background: The effect of initial epinephrine administration time from cardiac arrest on cerebral perfusion pressure (CePP) during CPR is controversial. The purpose of this study was to evaluate the association between initial epinephrine administration time and CePP in a porcine cardiac arrest model. Methods: Initial administration time of epinephrine was divided into 3 groups based on time after inducing ventricular fibrillation (VF): 5 minutes (early group), 10 minutes (intermediate group), and 15 minutes (delayed group). Twenty-four pigs were randomly assigned to each group. After 4 minutes of untreated ventricular fibrillation, 2 cycles of BLS (BLS1 and BLS2 phase) and 10 cycles of ACLS (ACLS1~10 phase) were conducted. Macrovascular circulation (CePP) and microvascular circulation using laser doppler flowmetry presented as a fraction of the baseline flow (f-LDF) were measured. Linear mixed model was used to measure median difference in CePP and f-LDF between groups. Results: A total of 22 pigs were analyzed. Early group showed higher and earlier peak of CePP and f-LDF compared to those of intermediate or delayed groups. There was a significant group by phase interaction in CePP where the early group showed a higher CePP on earlier phase. (Early group: median 38.2 [95% confidence intervals 30.7-50.5] mmHg at BLS 2 phase, intermediate group: 27.1 [14.1-35.7] mmHg at ACLS1 phase, late group: 12.2 [2.2-34.9] mmHg at ACLS 4 phase), p&lt; 0.001). There was no significant group by phase interaction in f-LDF; however, there was a tendency of decreased peak and delayed reach to peak with time. (Early group: median 5.7 [95% confidence interval 3.5-7.8] at ACLS 2 phase, intermediate group: 3.6 [1.5-5.1] at ACLS 4 phase, late group: 2.2 [0.9-3.3] at ACLS 6 phase, p =0.93). Conclusion: In this VF cardiac arrest porcine study, the early administration of epinephrine group showed higher and earlier peak of CePP and f-LDF compared to those of the intermediate and delayed groups.

Abstract 120: Impact Of Mask Application On Aerosol Generation During Chest Compression And Defibrillation In A Swine Cardiac Arrest Model

Introduction: We previously demonstrated that defibrillation followed by chest compression generates more aerosols than chest compression or no-flow state alone. However, the best strategies to prevent aerosol spread during cardiac arrest (CA) resuscitation remain unknown. We hypothesized that mask applications could reduce aerosol spread during chest compressions and defibrillation in a swine CA model. Methods: To simulate witnessed CA with bystander-initiated CPR, 24 female non-intubated swine (43.8 [2.7] kg) underwent 4 minutes of untreated ventricular fibrillation CA followed by 10 two-minute cycles of mechanical chest compression and defibrillation without ventilation. The animals were randomized to receive no mask, cloth mask, surgical mask, N95 mask, or a sealed nose cone over their snouts during resuscitation (n=5/group except nose cone n=4). The diameter (0.3 - 10 μm) and quantity of particles generated during 45-second intervals of no-flow, chest compression, and after each defibrillation were measured 2 inches anterior to the snout. Results: There were no significant differences between total particles generated during chest compression after defibrillation in unmasked versus masked animals regardless of the mask type, while the nose cone significantly reduced total particles. These findings were consistent across all 10 defibrillations (Fig. 1a) and all particle sizes (Fig. 1b). Furthermore, the minimal pre- and post-defibrillation particles detected outside of the nose cone indicated that the ineffectiveness of masks in preventing aerosol spread during CA resuscitation was likely due to their inadequate fit (Fig. 1c). Conclusion: Mask application did not reduce aerosol spread during defibrillation followed by chest compression in a swine CA model. Our data indicate that mask fit is a critical parameter for reducing aerosol transport and do not support mask application on CA victims during bystander-initiated CPR.