Agonal Breathing Research Articles

Sights and Sounds of Respiratory Changes During Hospice Death Vigils: Hospice Caregivers Experience

ContextResearch has documented common respiratory changes at the end of life for hospice patients. Some studies have noted these symptoms as distressing and challenging for families, and as a potential reason for emergency room visits and hospice benefit revocation. However, the experiences and emotions of family members regarding these respiratory changes in the final days, particularly when they are alone in a home setting, are not well documented. A recent study found 51% caregivers identified abnormal breathing as a challenge during their vigil experience. ObjectivesThe study aimed to answer three research questions: 1) How do family members describe the sights and sounds of the respiratory changes experienced during the final days of life? 2) What are the emotions caregivers experience as a result of witnessing the sights and sounds of respiratory changes? 3) What interventions are caregivers using to manage respiratory changes? MethodsA secondary analysis of 22 hospice caregiver interviews from a larger study of family interviews focused analyzing in depth narratives related to respiratory changes during the vigil period. Results Caregiver narrativesDistressful sights and sounds related to respiratory symptoms during the final days were described by 27% and 77% of family narratives, respectively. Negative emotional reactions were reported by more than a third of those interviewed. Caregivers expressed frustration at not understanding the reasons behind respiratory changes, with 27% noting they wished for more information on what to expect and how to intervene. There were inconsistencies in the interventions provided by hospice teams in managing respiratory symptoms. ConclusionsOpportunities exist for hospice agencies to better address the caregiver distress caused by witnessing noisy breathing (death rattle), Cheyne-Stokes breathing, and agonal breathing. Further research is needed to identify standard definitions for these respiratory changes, their prevalence in the home hospice setting, and to develop practice standards and effective interventions to relieve caregiver distress.

Uncovering Diaphragm Cramp in SIDS and Other Sudden Unexpected Deaths.

The diaphragm is the primary muscle of respiration. Here, we disclose a fascinating patient's perspective that led, by clinical reasoning alone, to a novel mechanism of spontaneous respiratory arrests termed diaphragm cramp-contracture (DCC). Although the 7-year-old boy survived its paroxysmal nocturnal "bearhug pain apnea" episodes, essentially by breathing out to breathe in, DCC could cause sudden unexpected deaths in children, especially infants. Diaphragm fatigue is central to the DCC hypothesis in SIDS. Most, if not all, SIDS risk factors contribute to it, such as male sex, young infancy, rebreathing, nicotine, overheating and viral infections. A workload surge by a roll to prone position or REM-sleep inactivation of airway dilator or respiratory accessory muscles can trigger pathological diaphragm excitation (e.g., spasms, flutter, cramp). Electromyography studies in preterm infants already show that diaphragm fatigue and sudden temporary failure by transient spasms induce apneas, hypopneas and forced expirations, all leading to hypoxemic episodes. By extension, prolonged spasm as a diaphragm cramp would induce sustained apnea with severe hypoxemia and cardiac arrest if not quickly aborted. This would cause a sudden, rapid, silent death consistent with SIDS. Moreover, a unique airway obstruction could develop where the hypercontracted diaphragm resists terminal inspiratory efforts by the accessory muscles. It would disappear postmortem. SIDS autopsy evidence consistent with DCC includes disrupted myofibers and contraction band necrosis as well as signs of agonal breathing from obstruction. Screening for diaphragm injury from hypoxemia, hyperthermia, viral myositis and excitation include serum CK-MM and skeletal troponin-I. Active excitation could be visualized on ultrasound or fluoroscopy and monitored by respiratory inductive plethysmography or electromyography.

8227 Complex Case of Myxedema Coma Complicated by Cardiac Arrest in a Geriatric Patient with Multiple Comorbidities

Abstract Disclosure: M. Parvez: None. L. Makahleh: None. S. Nagpal: None. A. Kavarthapu: None. V. Vedantam: None. Introduction: This case report details a rare instance of cardiac arrest in a patient with myxedema coma, a severe form of hypothyroidism. It highlights the diagnostic and therapeutic challenges in managing such complex endocrine emergencies. Case Presentation: A 70-year-old female with a history of hypothyroidism, type 2 diabetes, atrial fibrillation, pacemaker implantation, and COPD presented with a 3 day history of progressive lethargy and weakness. EMS found her with critically low blood glucose level of 20. History and Examination revealed non-compliance with thyroid medication and myxedematous features including moon-like facies, periorbital edema, generalized edema, elevated JVP, and cold extremities with sluggish capillary refill. In the ER, she was hypotensive, labs showed a significantly elevated TSH level of 30.55 (0.45-4.5), free T3 level of 1.2 (2.3-4.2), free T4 level of 1.12 (0.93-1.70), high lactate, metabolic acidosis, renal impairment, and liver enzyme elevation. These findings, coupled with the clinical presentation, led to the diagnosis of myxedema coma. The patient's critical state was further complicated by distributive shock, shock liver and oliguric AKI. Management included sodium bicarbonate infusion for severe acidosis, IV hydrocortisone, IV levothyroxine, and broad-spectrum antibiotics. Amiodarone was discontinued due to its potential contribution to acute liver injury and hypothyroidism. Despite interventions, she developed acute respiratory failure, requiring intubation and norepinephrine for low mean arterial pressure. Her renal function improved with pressor support, and her lactic acidosis resolved. She recovered quickly and was subsequently extubated. After stabilization, she was switched to oral levothyroxine and discharged. Shortly after discharge, she returned again with generalized weakness, confusion, and dysuria. ER evaluation revealed lethargy, hypotension, hypoglycemia, severe metabolic acidosis, and a UTI. She tested positive for Influenza. While in the ER, she had cardiac arrest, presenting with agonal breathing and PEA. CPR was initiated, achieving ROSC after two rounds and one dose of epinephrine. She was treated again with IV levothyroxine, and IV antibiotics. She recovered well and was discharged to rehab facility with re-education on compliance. Conclusion: This case exemplifies the complexity and challenges in managing a geriatric patient with multiple comorbidities, particularly in the context of myxedema coma. The intricate interplay of endocrine, cardiovascular, respiratory, and infectious complications necessitated a multifaceted and dynamic therapeutic approach. This case underscores the importance of compliance, vigilant monitoring, prompt recognition of complicating factors, and the need for a coordinated multidisciplinary approach in managing similar cases. Presentation: 6/2/2024

Acute respiratory compromise in the NICU

Acute respiratory compromise (ARC) is a significant and frequent emergency in the Neonatal Intensive Care Unit (NICU), characterized by absent, agonal, or inadequate respiration that necessitates an immediate response. The primary etiologies of ARC in neonates can be categorized into upper and lower airway issues, disordered control of breathing, and lung tissue disease. ARC events are particularly dangerous as they compromise oxygen delivery and carbon dioxide removal, potentially leading to cardiopulmonary arrest. Approximately 1 % of NICU admissions experience cardiopulmonary arrest, and ARC is the primary cause of most events. This article provides a comprehensive review of the etiologies of ARC, including anatomical abnormalities, syndromic disorders, airway obstruction, and pulmonary diseases such as bronchopulmonary dysplasia and pneumonia. Management strategies include the use of continuous positive airway pressure, positive pressure ventilation, and advanced interventions like extracorporeal membrane oxygenation (ECMO) in cases of severe respiratory distress. Additionally, quality improvement initiatives aimed at reducing incidents such as unplanned extubations (UE) are discussed, along with emergency responses to ARC, which often require multidisciplinary collaboration and advanced airway management. The article emphasizes the importance of preparedness, training, and structured emergency protocols to ARC in the NICU to optimize patient care.

Abstract A099: Pulmonary thromboembolism secondary to iron deficiency anemia: A case study

Abstract Introduction: Pulmonary thromboembolism (PTE) is a significant clinical issue associated with high morbidity and mortality. Risk factors for thromboembolic events include immobilization, myocardial infarction, cerebrovascular accident, surgery, and trauma. Iron deficiency anemia (IDA) can cause reactive thrombocytosis, increasing thromboembolic risk. This study presents a 30-year-old female admitted for PTE, possibly secondary to IDA. Case Presentation: A 30-year-old female with IDA and heavy menstrual bleeding presented with right-sided chest pain and shortness of breath. Her pain, exacerbated by inspiration, and relieved by leaning forward, had worsened over four days. She also reported dizziness and agonal breathing. On arrival, her vitals included a blood pressure of 95/62 mmHg, heart rate of 110 bpm, respiratory rate of 22 breaths/min, and a temperature of 37°C. Physical examination revealed tachycardia, tachypnea, and diminished breath sounds in the right lower lung field. Laboratory tests showed a hemoglobin level of 4.6 g/dL and a platelet count of 745 × 10^9/L, low ferritin, low serum Iron, and high total iron-binding capacity (TIBC). A CT pulmonary angiogram revealed a wedge-shaped infarct in the right lower lobe, consistent with pulmonary embolism. CT abdomen/pelvis showed a thrombus in the right iliac vein, indicative of deep vein thrombosis. The echocardiogram showed left ventricular ejection fraction >55% with no right chamber strain. A pelvic ultrasound revealed no significant pathology. Treatment included heparin and blood transfusions, increasing hemoglobin to 9.0 g/dL. Hemolytic workup including prothrombin gene abnormalities, Factor V Leiden mutation, and protein C activity was negative. However, Protein S activity was low, and PTT-la positive, implying that the patient may be positive for lupus anticoagulant, later ruled out by serial antibody tests.Subsequently, the patient was discharged home on Eliquis and Ferrous sulfate with outpatient hematology follow-up. Discussion: The association between venous thromboembolism and IDA can be explained by several mechanisms. One study suggests that iron deficiency causes hypercoagulability through reactive thrombocytosis, increased oxidative stress, and altered blood viscosity. Another hypothesis is that the hyperdynamic state in anemic patients leads to vascular endothelial injury due to shear forces. This case highlights the importance of considering IDA as a potential risk factor for thromboembolism, especially in patients without other evident prothrombotic conditions. Conclusion: Iron deficiency may be an underestimated risk factor for thromboembolic events. This case underscores the need for a comprehensive workup for VTE that includes assessing for IDA. Iron replacement therapy could serve as an effective preventive strategy in patients with a history of IDA and those at risk for thromboembolism. Further research is warranted to explore the mechanisms linking IDA with increased thrombotic risk and to establish appropriate preventive measures. Citation Format: Aliya M Khan, Maria Toustsoglou, Sandy Philippeaux, David Del sol, Mehmet Hepgur. Pulmonary thromboembolism secondary to iron deficiency anemia: A case study [abstract]. In: Proceedings of the 17th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2024 Sep 21-24; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2024;33(9 Suppl):Abstract nr A099.

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.

Abstract 254: Patients With Signs of Life on Hospital Arrival Have a Higher Chance of Survival and Favorable Neurological Outcomes Following Traumatic Cardiac Arrest

Introduction: The clinical impact of signs of life (SOL) in traumatic cardiac arrest (TCA) remain to be elucidated. A previous study compared TCA patients with pulseless electrical activity (PEA) to those with asystole, but survival was not significantly different between the groups. Other obvious SOL (i.e., fine extremity/eye movement, light reflection, agonal respiration) have not yet been examined in TCA. Hypothesis: We hypothesized that TCA patients with SOL on hospital arrival have a higher chance of survival and good neurological outcomes. Aim: To examine survival and neurological outcomes in TCA patients with or without SOL. Methods: Retrospective review of data from the Japan Trauma Data Bank (2019-2021). The inclusion criteria were patients with TCA on arrival. The exclusion criteria were patients with burns, abbreviated injury scale score> 6 in any region, and missing survival or SOL data. SOL was defined as follows: extremity or eye movement, light reflex, gasping, pulseless electrical activity with electrical heart activity > 40 beats per minute. The primary outcome was survival at discharge. The secondary outcome was favorable neurological outcome (Glasgow Outcome Scale score of 4 or 5) at hospital discharge. Patients with and without SOL were compared using univariable analysis. Results were described with odds ratio (ORs) and 95% confidence intervals (CI). Results: A total of 2,136 patients (121 with SOL and 2,015 without SOL) were included. The characteristics of patients with or without SOL were as follows: age (median age 60.5 years old [interquartile range: 42-80 years] vs. 55.2 [38-75]), gender (male: 83/121 (68.6%) vs. 1,321/2,015 (65.9%), Injury Severity Score (32.9 [22-43] vs. 33.7 [22-41]), blunt trauma (97/121 (82.2%) vs. 1,711/2,015 (84.9%)), and transportation time (15.1 min [7-18] vs. 13.3 [7-16]). The patients with SOL showed higher survival compared with the patients without SOL (11/121 (8.5%) vs. 24/2015 (1.2%), OR 1.9 [CI 1.38-2.85]). A similar trend was observed for favorable neurological outcomes (5/95 (5.3%) vs. 7/1,440 (0.5%), OR 2.41 [CI 1.26-3.60]). Conclusions: TCA patients with SOL at arrival showed higher survival and favorable neurological outcomes at hospital discharge compared with TCA patients without SOL.

Abstract 17127: Rapid Progression of Conduction System Disease in Suspected Fulminant Nivolumab Myocarditis

Background: Immune checkpoint inhibitors (ICI) have shown efficacy in treating a wide spectrum of malignancies, but have a known risk of cancer therapy related cardiac toxicity. We present a case that demonstrates how conduction system disease can rapidly progress in a patient with suspected nivolumab (PD1) induced fulminant myocarditis. Case: An 82-year-old male with a history of esophageal carcinoma presented with agonal breathing and altered mental status. He had received his second dose of PD1 therapy three days prior. He was intubated and admitted for hypoxic respiratory failure and elevated troponin. His initial EKG demonstrated new marked 1st degree AV block with right bundle branch block (RBBB) morphology. A stat echocardiogram noted an EF of 60-65% with no wall motion abnormalities. Decision-making: On Day 2, Mobitz Type I block was appreciated on telemetry. The patient met criteria for acute myocarditis with his clinical presentation, new conduction system disease, and high sensitivity troponin of 13,000. Given recent PD1 therapy, lack of infectious prodrome, and lack of prior heart disease, suspicion for ICI induced myocarditis was high. High dose steroid therapy was initiated. On Day 3, the patient was noted to have alternating left bundle branch block and RBBB. On Day 4, he progressed to complete heart block, prompting transvenous pacemaker (PM) placement with subsequent permanent PM placement. A repeat echo showed global hypokinesis with an EF of 40-45% and reduced RV function. He also required vasopressor support meeting criteria for fulminant myocarditis. Due to his hemodynamic instability and low clinical suspicion, he did not receive cardiac catheterization. Cardiac MRI and cardiac biopsy were not readily available in this institution. Conclusion: The clinical findings, lack of infectious prodrome, and worsening arrhythmia requiring pacing and vasopressor support, in patient with recent PD1 treatment suggests nivolumab induced fulminant myocarditis. In institutions without advanced testing infrastructure, rapid recognition of progressive conduction system disease may be used as an early marker for diagnosis, treatment initiation, and referral to tertiary care centers for advanced management of fulminant ICI myocarditis.

346 A Novel Algorithm to Recognize Agonal Respiration for Emergency Call of Cardiac Arrest Dispatch

346 A Novel Algorithm to Recognize Agonal Respiration for Emergency Call of Cardiac Arrest Dispatch

Video characteristics for remote recognition of agonal respiration: A pilot study

AimThe mobile network quality in ambulances can be variable and limited. This pilot study aimed to identify a suitable network setting for recognizing agonal respiration under limited network conditions. MethodsWe recruited five emergency medical technicians, and each participant viewed 30 real-life videos with different resolutions, frame rates, and network scenarios. Thereafter, they reported the respiration pattern of the patient and identified agonal respiration cases. The time at which agonal respiration was identified was also recorded. The answers provided by the five participants were compared with those of two emergency physicians to compare the accuracy and time delay in breathing pattern recognition. ResultsThe overall accuracy for initial respiratory pattern recognition was 80.7% (121/150). The accuracy for normal breathing was 93.3% (28/30), for not breathing was 96% (48/50), and for agonal breathing was 64.3% (45/70). There was no significant difference in successful recognition between video resolutions. However, the rate of time delay in recognizing agonal respiration less than 10 seconds between 15-fps group and 30-fps group had statistical significance (21% vs 52%, p = 0.041). ConclusionThe frame rate emerges as one of critical factors in agonal respiration recognition through telemedicine, outweighing the significance of video resolution.

PO-04-053 OUT-OF-HOSPITAL CARDIAC ARREST ASSOCIATED WITH EARLY REPOLARIZATION

Early repolarization syndrome (ERS) is characterized by J-point elevation presenting as slurring or notching of the terminal part of the QRS complex. Of the several congenital and acquired disorders that encompass J-wave syndromes, ERS has been linked to increased risk of developing polymorphic VT and idiopathic VF that can lead to sudden cardiac death. To describe a patient who presented after a cardiac arrest with initial ECG criteria consistent with Type III ERS who recieved a dual-chamber ICD. n/a We present a case of a 42-year-old man without any prior history that presented to the emergency room after successful resuscitation from out-of-hospital cardiac arrest due to VF. After noticing agonal respiration during early morning hours, his wife called emergency medical services (EMS) and promptly performed cardiopulmonary resuscitation. Upon arrival, EMS found the patient to be in VF. He was shocked once by an automatic external defibrillation leading to ROSC with restoration of sinus rhythm. In the ED, his initial vitals were 122/93 mmHg, 104 bpm, 95% oxygen saturation on room air, and temperature of 36.4 °C. He denied any family history of sudden cardiac death. Wife reported prior history of nocturnal agonal respirations. Initial diagnostic work-up was significant for a leukocytosis of 19,000 and serial high-sensitivity cardiac troponins of 130, 305, and 364 with a 0/3-hour delta change of 234. A12-lead ECG upon presentation is shown in Figure 1 without previous ECGs available for comparison. An emergent coronary angiography was performed which revealed no significant coronary obstruction or anomaly. With both his ECG findings and a Shanghai Score of 7, a diagnosis of Type III ERS was highly suspected. Further diagnostic testing included a TTE showing left ventricular dysfunction with an ejection fraction of 40-45%. CMR showed no delayed gadolinium enhancement. Ultimately, a dual-chamber ICD was implanted during the admission. Follow-up ECGs revealed resolution of slurred terminal QRS complexes. He was discharged on beta blocker and low-dose losartan with close outpatient follow-up with electrophysiology. ECG changes of ERS can be dynamic and may sometimes be concealed, particularly in the setting of an out-of-hospital cardiac arrest. It is important to identify early repolarization patterns due to the adverse prognostic significance especially of Type III ERS which is associated with the highest level of risk for development of malignant arrhythmia.

Hemihydranencephaly of Premature Infant - Case Report

Abstract Hydranencephaly represents a rare anomaly of the central nervous system and is characterized by the parenchymal absence which is replaced with a membranous sac filled with cerebrospinal liquid, glial tissue and ependyma. When it is manifested as hemihydranencephaly, the patient’s prognosis is better. We presented a case of a premature infant with hemihydranencephaly in twin pregnancy that had a fatal outcome. A premature infant in a controlled pregnancy was delivered at 31 weeks of gestational age. The mother of the newborn was hospitalized in the Clinic for Infective Diseases since she had tested positive for SARS-Covid- 19. Following an urgent Caesarean section, the newborn was tested for Covid 19 using the rapid antigen and PCR test and the results were negative. In the delivery room, the tactile stimulation, aspiration, positive pressure ventilation of the infant were applied, after which it was intubated. After the intubation, a manual heart massage was performed, after which the cardiac activity and agonal breathing movements were detected.” Three hours later, cardiorespiratory arrest happened, following unsuccessful resuscitation. The other twin was born with no anomalies, but showed signs of respiratory distress syndrome. Autopsy revealed that there was a thin-walled cavity filled with clear, yellowish liquid in the right hemisphere. Documenting cases of newborns with hydranencephaly is of a great importance for counseling parents regarding length of survival, successful management of pregnancy, and performance of prenatal diagnostic procedures.

Woman with agonal breathing.

A 42-year-old healthy woman with cerebral palsy, oriented consciousness, and partial dependence in daily activities at baseline reported gradual decrease in muscle strength in all her limbs for 6 months. The patient became comatose with agonal breathing unexpectedly during the night hours without any warning. Initial clinical presentation showed a very slow respiratory rate of 8 times/min and SpO2 = 92% under non-rebreathing mask covering. Atrial blood gas test revealed hypercapnic respiratory acidosis (pH, 6.9; PCO2 > 200 mmHg). Intubation was performed immediately. Chest radiography showed no active lesions (Figure 1). Her consciousness returned to baseline a few hours after intubation, but she developed quadriplegia. Brain computed tomography showed no obvious lesions. Brain magnetic resonance imaging (MRI) revealed no obvious lesion but incidentally revealed C2 odontoid process fracture with cord indentation (Figure 2). Cervical MRI showed displaced odontoid process fracture with cord compression, causing myelopathy at C2–C4 levels (Figure 3). It is challenging to diagnose spinal cord injury (SCI) in the absence of trauma history.1 Non-traumatic SCI is a rare neurological emergency.2 There are few case reports of spontaneous atraumatic cervical fracture due to tuberculosis or rheumatoid arthritis.3, 4 High-level SCI causes impairment of respiratory muscles and reduces vital capacity and chest wall compliance. It also influences the respiratory drive, leading to hypercapnia.5, 6 SCI is an often forgotten but important cause of central nervous system depression in patients with hypercapnic respiratory failure in emergency settings. We present a case of atraumatic odontoid fracture, resulting in myelopathy and hypercapnic respiratory failure. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Saved by point of care echo.

A 40-year-old black male with a past medical history of sickle cell disease, cardiomyopathy, and pulmonary hypertension presents as a transfer from an outside facility to a tertiary care hospital for evaluation after a formal echocardiogram reported “biatrial enlargement and small cystic structure adjacent to the right atrium.” The patient arrived at the receiving hospital in acute severe distress with altered mental status, tachycardia, tachypnea, hypoxia, and hypotension with near agonal respirations on bilevel positive airway pressure. He was also noted to have bilateral jugular venous distention to the angle of mandibles and bilateral lower extremity edema. Given the acuity of the patient's condition, a bedside point-of-care (POC) ultrasound was done using the Rapid Ultrasound for Shock and Hypotension (RUSH) protocol. Bilateral lung slide was present with a bilateral A-line profile. Inferior vena cava (IVC) interrogation showed a markedly dilated non-distensible IVC. In the apical 4-chamber cardiac view, with color Doppler, it became obvious that there was a very large extracardiac cystic mass nearly completely compressing the right atrium (Video 1). Mitral valve inflow velocity was assessed via pulse wave Doppler and was found to demonstrate echocardiographic pulsus paradoxus (Figure 1). The emergency physician made the diagnosis of an extracardiac cystic mass compressing the right atrium causing pericardial tamponade rapidly at the bedside. A multidisciplinary team was mobilized by the emergency physician and the epicardial cyst was drained under ultrasound guidance in the emergency department resulting in 1300 cc of serous fluid with the restoration of the right atrium volume, normalization of the patient's vital signs, and return to his normal mental status. Pericardial tamponade occurs when there is an impairment of ventricular filling due to atrial compression by pericardial fluid or blood.1 Far more rarely, cardiac tamponade can be caused by extrinsic compression.2 Traumatic pericardial effusions typically occur rapidly and present as acute hemodynamic compromise in the setting of trauma. Medical causes of tamponade can be much more insidious given the usually slower accumulation of pericardial fluid. Pericardial tamponade presents typically as either cardiogenic or obstructive shock. Although physical exam findings such as Beck's triad, are often cited, echocardiography provides an invaluable tool in the detection of tamponade.3 In one case series, the sensitivity of the presence of all 3 components of Becks Triad was 0%, whereas any single element had a sensitivity 50%.4 Emergency physicians can rapidly diagnose pericardial tamponade with POC ultrasound and thus render lifesaving treatment, as in this case.

Artificial hypobiosis as a method of acute altitude illness negative impact reduction

Introduction. Critical stage of acute mountain (altitude) sickness, manifesting by loss of consciousness, convulsions, apnea and high risk of death, develops at altitudes above 8 km. Acute oxygen starvation of the central nervous system while significant hypobaric hypoxia is the main mechanism of critical stage of acute mountain sickness. Alpinists and professional guides, extreme athletes are the main risk group. It is proposed to reduce the level of metabolism (artificial hypobiosis induction) to prevent the negative impact of acute hypobaric hypoxia on central nervous system. The study aims to assess the efficiency of the metabolic rate reduction for the organism negative impact prevention while acute hypobaric hypoxia. Materials and methods. Study had 2 stages. The 1st - definition of the possibility of using artificial hypobiosis model. The 2nd - the model efficiency definition. Syrian hamsters 90-110 g weight were used in the study. 5 groups, 8 animals in each. Animals of two experimental groups (1 - on the 1st stage and 1 - is on the 2nd) had intramuscular injections of 1 g/kg Methyldopa (CAS Number 555-30-6). Animals control groups (1 - on the 1st stage and 2 - is on the 2nd) had 0,9% NaCl. Indirect calorimetry was performed on the 1st stage. Oxygen consumption and carbon dioxide elimination speed were measured in each animal group twice: before intramuscular injection and 3 hours after. Critical stage of acute mountain (altitude) sickness was performed on the 2nd stage. In 3 hours after intramuscular injection animals of each group had been placed in hypobaric chamber. 30 kPa underpressure for control group #1 animals and 20 kPa for control group #2 and experimental group animals, speed - 1,25 kPa/s. To avoid CO2 accumulation continuous chamber air flow was made. Continuous visual observation carried out. Consciousness, posture maintenance time, convulsive seizures, agonal breathing, and apnea were registered. Results. 1st stage. Experimental group animals’ mean base oxygen consumption speed was 4,04±0,3 ml/100 g/min, and 2,70±0,11 ml/100 g/min (p<0,01) after intramuscular injection., carbon dioxide elimination speed was 3,17±0,27 ml/100 g/min and 2,26±0,09 ml/100 g/min (p<0,01) respectively. Control group animals’ mean base oxygen consumption speed was 3,80±0,43 ml/100 g/min, and 3,88±0,37 ml/100 g/min after intramuscular injection, carbon dioxide elimination speed was 2,95±0,31 ml/100 g/min and 2,92±0,2 ml/100 g/min, respectively. 2nd stage. 20 kPa control group: since start of exposure the average animal posture maintenance time was 3±2 s, the first convulsion time - 20±3 s, the second convulsion - 56±5 s, agonal breath start - 52±9 s, apnea - 114±26 s. Consciousness absence in all animal was observed. Experimental group: none of the parameters is to register were observed. All animals had consciousness, actively restored their position, while chamber was tilted. The exposure lasted for 20 minutes. 30 kPa control group: 1 animal of 8 had convulsions on 56 s of 20-minute exposure. None of the parameters is to register were observed in other animals. All animals had consciousness, actively restored their position, while chamber was tilted. Conclusions. The effectiveness of lowering the metabolic rate for the prevention of loss of consciousness and the development of generalized convulsions in acute hypobaric hypoxia has been experimentally proven; in a state of artificial hypobiosis, the time of safe stay in a hypoxic environment increases by more than 20 times. Ethics. The study was carried out in accordance with the ethical principles of the Declaration of Helsinki. The Clinical Study Protocol was reviewed at a meeting of the local Ethics Committee FSBSI IRIOH.

Barriers to the Initiation of Telecommunicator-CPR during 9-1-1 Out-of-Hospital Cardiac Arrest Calls: A Qualitative Study

Introduction Fewer than 10% of individuals who suffer out-of-hospital cardiac arrest (OHCA) survive with good neurologic function. Bystander CPR more than doubles the chance of survival, and telecommunicator-CPR (T-CPR) during a 9-1-1 call substantially improves the frequency of bystander CPR. Objective We examined the barriers to initiation of T-CPR. Methods We analyzed the 9-1-1 call audio from 65 EMS-treated OHCAs from a single US 9-1-1 dispatch center. We initially conducted a thematic analysis aimed at identifying barriers to the initiation of T-CPR. We then conducted a conversation analysis that examined the interactions between telecommunicators and bystanders during the recognition phase (i.e., consciousness and normal breathing). Results We identified six process themes related to barriers, including incomplete or delayed recognition assessment, delayed repositioning, communication gaps, caller emotional distress, nonessential questions and assessments, and caller refusal, hesitation, or inability to act. We identified three suboptimal outcomes related to arrest recognition and delivery of chest compressions, which are missed OHCA identification, delayed OHCA identification and treatment, and compression instructions not provided following OHCA identification. A primary theme observed during missed OHCA calls was incomplete or delayed recognition assessment and included failure to recognize descriptors indicative of agonal breathing (e.g., “snoring”, “slow”) or to confirm that breathing was effective in an unconscious victim. Conclusions We observed that modifiable barriers identified during 9-1-1 calls where OHCA was missed, or treatment was delayed, were often related to incomplete or delayed recognition assessment. Repositioning delays were a common barrier to the initiation of chest compressions.

Novel SCN5A and GPD1L Variants Identified in Two Unrelated Han-Chinese Patients With Clinically Suspected Brugada Syndrome.

Brugada syndrome (BrS) is a complexly genetically patterned, rare, malignant, life-threatening arrhythmia disorder. It is autosomal dominant in most cases and characterized by identifiable electrocardiographic patterns, recurrent syncope, nocturnal agonal respiration, and other symptoms, including sudden cardiac death. Over the last 2 decades, a great number of variants have been identified in more than 36 pathogenic or susceptibility genes associated with BrS. The present study used the combined method of whole exome sequencing and Sanger sequencing to identify pathogenic variants in two unrelated Han-Chinese patients with clinically suspected BrS. Minigene splicing assay was used to evaluate the effects of the splicing variant. A novel heterozygous splicing variant c.2437-2A>C in the sodium voltage-gated channel alpha subunit 5 gene (SCN5A) and a novel heterozygous missense variant c.161A>T [p.(Asp54Val)] in the glycerol-3-phosphate dehydrogenase 1 like gene (GPD1L) were identified in these two patients with BrS-1 and possible BrS-2, respectively. Minigene splicing assay indicated the deletion of 15 and 141 nucleotides in exon 16, resulting in critical amino acid deletions. These findings expand the variant spectrum of SCN5A and GPD1L, which can be beneficial to genetic counseling and prenatal diagnosis.

Pregnancy in women with Brugada syndrome: Is there an increased arrhythmia risk? A case-series report.

In some rare arrhythmia syndromes, arrhythmia risk in female patients increases during pregnancy, necessitating extra controls. We wanted to evaluate if the increased risk for arrhythmia during pregnancy applies in women with Brugada syndrome and their potentially affected fetuses. A comprehensive literature search was performed on PubMed (MeSH search terms "Brugada syndrome,""pregnancy,""parturition,""labor,""delivery,""fetal death," and "stillbirth"). Overall, six case reports with a total of six patients were identified. Of these six patients (three carriers of an SCN5A variant, three not tested), two women (both with unknown SCN5A status), developed severe cardiac events during pregnancy. The first patient, with a previous history of aborted sudden cardiac arrest at the age of 12 years, developed ventricular fibrillation(VF), while the other was diagnosed with Brugada syndrome postpartum because of nocturnal agonal respiration during pregnancy. These (limited, heterogenous) cases suggest that women with Brugada syndrome (and their possibly affected fetuses), might have an overall low tendency to develop arrhythmias during pregnancy, but important data on risk factors (SCN5A status) are lacking. Arrhythmia risk during pregnancy seems to increase in probands and those who have previously experienced cardiac events. We suggest the use of risk stratification in these women to improve patient care, lower the emotional stress and physical burden for the pregnant mother, and lower health costs. Furthermore, we plead for SCN5A analysis in all these women for use of risk stratification and to enable cascade screening especially for specialized care in children carrying an SCN5A mutation.

Family screening in brugada syndrome patients

Abstract Background Brugada syndrome (BS) is a rare inherited channelopathy associated with sudden cardiac death (SCD) and family screening (FS) of index patients (pts) is recommended. However, data about pts identified through FS is lacking. Aim To compare index pts to non-index pts identified through systematic FS. Methods Single-center retrospective study of BS pts followed by the Arrhythmology Department. FS was offered to 1st degree relatives of all index pts through primary care services and a once-weekly voluntary open appointment. Genetic counselling was performed when indicated. Index and non-index pts were compared regarding baseline characteristics and events during the follow-up (syncope of probable arrhythmic origin, ventricular tachycardia/ventricular fibrillation (VT/VF) and SCD). Results We included 165 pts (61% males, mean age 47±15 years) and 72 (44%) were identified through FS. Non-index pts were diagnosed at a younger age (42±14 vs 51±14 years, p <.001), were more often female (57% vs 25%, p<.001), were diagnosed predominantly through provocative test with ajmaline/flecainide (88% vs 47%, p<.001) and had less documented spontaneous type 1 ECG pattern (17% vs 59%, p<.001). A type 2 pattern was identified in 18 (25%) non-index pts. Genetic testing was performed in 38 (53%) non-index pts: 6 had a pathogenic SCN5A mutation, 18 a likely pathogenic SCN5A mutation and 12 a mutation of uncertain significance. At diagnosis, 24 (33%) non-index pts had history of syncope, 3 (4%) had nocturnal agonal respiration and 11 (15%) had palpitations with no differences between both groups (p=.119). Non-index pts were less likely to implant a cardioverterdefibrillator (14% vs 38%, p=.001). During a median follow-up of 28 (IQR 16–41) months, 10 (6%) pts had an event - 2 (3%) in the non-index group (2 syncope) and 8 (9%) in the index group (1 syncope; 7 VT/VF) - with no significative differences between groups (p=.432). There were nocardiovascular deaths. Conclusions FS identified a considerable proportion of BS pts. Non-index pts were younger at the time of the diagnosis and had less spontaneous type 1 pattern. No differences were found in events between index and non-index pts, however, the event rate was low. Systematic FS can identify individuals at risk of SCD earlier, allowing close monitoring and, when indicated, appropriate treatment. Funding Acknowledgement Type of funding sources: None.

Assessment of breathing in cardiac arrest: a randomised controlled trial of three teaching methods among laypersons

BackgroundThe aim of this trial was to compare a video- and a simulation-based teaching method to the conventional lecture-based method, hypothesizing that the video- and simulation-based teaching methods would lead to improved recognition of breathing patterns during cardiac arrest.MethodsIn this Danish, investigator-initiated, stratified, randomised controlled trial, adult laypersons (university students, military conscripts and elderly retirees) participating in European Resuscitation Council Basic Life Support courses were randomised to receive teaching on how to recognise breathing patterns using a lecture- (usual practice), a video-, or a simulation-based teaching method. The primary outcome was recognition of breathing patterns in nine videos of actors simulating normal breathing, no breathing, and agonal breathing (three of each). We analysed outcomes using logistic regression models and present results as odds ratios (ORs) with 95% confidence intervals (CIs) and P-values from likelihood ratio tests.ResultsOne hundred fifty-three participants were included in the analyses from February 2, 2018 through May 21, 2019 and recognition of breathing patterns was statistically significantly different between the teaching methods (P = 0.013). Compared to lecture-based teaching (83% correct answers), both video- (90% correct answers; OR 1.77, 95% CI: 1.19–2.64) and simulation-based teaching (88% correct answers; OR 1.48; 95% CI: 1.01–2.17) led to significantly more correct answers. Video-based teaching was not statistically significantly different compared to simulation-based teaching (OR 1.20; 95% CI: 0.78–1.83).ConclusionVideo- and simulation-based teaching methods led to improved recognition of breathing patterns among laypersons participating in adult Basic Life Support courses compared to the conventional lecture-based teaching method.