Bedside Echocardiogram Research Articles

Cardiogenic shock in phaeochromocytoma multisystem crisis- a case report

Abstract Background Phaeochromocytoma multisystem crisis (PMC) is characterised by labile blood pressures (extremes of hypo- and/or hypertension) and multiorgan failure as a result of catecholamine excess. Initial stabilisation requires pharmacological and/or mechanical circulatory support, followed by institution of antihypertensives to correct the underlying pathophysiology. Case summary A previously well 40-year-old male developed sudden onset of breathlessness. On presentation, he was in shock with multiorgan failure. He required intubation, mechanical ventilation, dual inotropic support and renal replacement therapy. Bedside echocardiogram showed a severely impaired left ventricular ejection fraction (LVEF) of 25%. Coronary angiography revealed normal coronary arteries. In view of raised inflammatory markers and transaminitis, a CT abdomen/pelvis was performed. An incidental left adrenal mass was found. Further work-ups revealed raised plasma metanephrine and normetanephrine, 24-hour urine epinephrine and norepinephrine. A cardiac magnetic resonance (CMR) showed myocardial inflammation and reverse Takotsubo pattern of regional wall motion abnormality (RWMA). The diagnosis of cardiogenic shock and stress cardiomyopathy secondary to phaeochromocytoma multisystem crisis was made. He was subsequently initiated on α- and β-blockers and goal-directed medical therapy for heart failure. A 68Ga-DOTATATE scan showed avid tracer uptake of the left phaeochromocytoma. An interval CMR 3 weeks from presentation showed near normalisation of the LVEF and RWMA. He underwent a successful laparoscopic left adrenalectomy and was antihypertensive-free since. Conclusion The clinical suspicion for PMC as the cause of cardiogenic shock requires astute clinical judgement, while the management requires understanding of the underlying pathophysiology that call for multidisciplinary inputs.

Right Ventricular “Bubble Time” to Identify Patients With Right Ventricular Dysfunction

ObjectiveWe propose a novel method of evaluating right ventricular (RV) dysfunction in the emergency department (ED) using RV “bubble time” – the duration of time bubbles from a saline flush are visualized in the RV on echocardiography. The objective was to identify the optimal cutoff value for RV bubble time that differentiates patients with RV dysfunction and report on its diagnostic test characteristics. MethodsThis prospective diagnostic accuracy study enrolled a convenience sample of hemodynamically stable ED patients. A sonographer administered a 10-milliliter saline flush into patient’s intravenous catheter, performed a bedside echocardiogram, and measured RV bubble time. Subsequently, the patient underwent a comprehensive cardiologist-interpreted echocardiogram with 36 hours, which served as the gold standard. Patients with RV strain or enlargement on the latter echocardiogram were considered to have RV dysfunction. Bubble time was evaluated by a second provider, blinded to the initial results, who reviewed the ultrasound clips. The primary outcome measure was the optimal cutoff value of RV bubble time that identifies patients with and without RV dysfunction. ResultsOf 196 patients, median age was 67 and half were female, with 69 (35.2%) having RV dysfunction. Median RV bubble time among patients with RV dysfunction was 62 seconds (interquartile range (IQR): 52, 93) compared with 21 seconds (IQR: 12, 32) among patients without (p<0.0001). The optimal cutoff value of RV bubble time for identifying patients with RV dysfunction was ≥40 seconds, with a sensitivity of 0.97 (95% CI: 0.93, 1.00) and specificity of 0.87 (95% CI: 0.82, 0.93). ConclusionIn ED patients, an RV bubble time of ≥40 seconds had high sensitivity in identifying patients with RV dysfunction, while an RV bubble time of <40 seconds had good specificity in identifying patients without RV dysfunction. These findings warrant further investigation in undifferentiated patient population and by emergency physicians without advanced ultrasound training.

Carbon monoxide poisoning manifesting with rhabdomyolysis, Takotsubo syndrome, and skin lesion: A case report

Carbon monoxide (CO) poisoning is characterized by non-specific and protean clinical manifestations, exhibiting a highly variable presentation. We present a case of an 83-year-old female Alzheimer&amp;rsquo;s patient, a non-smoker, who was found unconscious in her wheelchair by her caregiver at home. The heating in the apartment was powered by liquefied petroleum gas. On admission to the emergency department, her vital signs were normal, but she was unconscious and slightly dyspneic. The examination revealed red-colored skin lesions in the submammary area, where the wheelchair safety belt was firmly fastened. The rest of the physical examination results were unremarkable. The carboxyhemoglobin level was 23%, and there was an increase in creatine phosphokinase and troponin I levels. On the 2nd day of hospitalization in the emergency ward, the electrocardiogram revealed negative T waves in the V1&amp;ndash;V6 leads, while the bedside echocardiogram revealed apical ballooning of the left ventricle. The myocardial perfusion examination yielded a negative result for myocardial ischemia. In the management of patients with CO poisoning, it is important for emergency physicians to assess the presence of multiple organ and tissue disorders. Consequently, the patient was diagnosed with CO poisoning with skin, skeletal, and cardiac muscle involvement.

Intra-pericardial thrombin injection in iatrogenic cardiac tamponade: a case report

BackgroundNowadays, percutaneous procedures are expanding in use, and this comes with complications associated with the procedure itself. Cardiac tamponade is rare but may be life threatening since it can involve hemodynamic instability. It is known that after pleural effusion during a percutaneous procedure, pericardiocentesis should be used as drainage of the cavity. However, that does not achieve hemostasis in some cases, and in those patients who are hemodynamically unstable, a sealing agent to promote hemostasis might be useful, like thrombin.Case presentationWe present a case report of 89-year-old patient with history of melanoma undergoing treatment with pembrolizumab, who attended the emergency department referring chest pain (intensity 5/10) and palpitations that have lasted hours. He had TnTUs 554/566 ng/L and an echocardiogram that showed dilated right chambers, hypertrophy and global hypokinesia of the left ventricle, increased filling pressures of the left ventricle and pulmonary hypertension. Myocarditis associated with pembrolizumab was suspected, so high dose steroids were initiated and endomyocardial biopsy was conducted, resulting in iatrogenic cardiac tamponade. To determine the etiology of the suspected myocarditis, an endomyocardial biopsy was performed. Unfortunately, an intraprocedural complication arose: pleural effusion resulting in iatrogenic cardiac tamponade, leading to hemodynamic instability. It required immediate pericardial drainage via subxiphoid puncture, obtaining a 550 mL hematic debit. Clinical manifestations raised suspicion of tamponade, prompting a bedside echocardiogram for a definitive diagnosis. Despite these efforts, the patient remained hemodynamically unstable, and due to the elevated surgical risk, intrapericardial thrombin was employed to achieve successful hemostasis.ConclusionsCardiac tamponade is a life-threatening condition that can sometimes be induced iatrogenically, resulting from percutaneous interventions. Despite limited evidence regarding this therapeutic strategy, in patients experiencing iatrogenic cardiac tamponade with hemodynamic instability and high surgical risk, the administration of intra-pericardial thrombin could be contemplated.

Abstract 15948: Highly Suspicious Yet Diagnostically Unrevealing Left Ventricular Free-Wall Rupture Following STEMI

Introduction: Left ventricular wall rupture is a rare but lethal complication following a ST elevation myocardial infarction (STEMI). We present a case of left ventricular free-wall rupture not identified on echocardiography and CT angiography (CTA) despite high suspicion who underwent emergent lifesaving mediastinal exploration and repair. Case: A 52-year-old male with past medical history of hypertension presented with typical chest pain. He was found to have STEMI with 100% left anterior descending (LAD) artery occlusion and underwent percutaneous coronary intervention to mid LAD. Post procedure, he developed atrial fibrillation with rapid ventricular rate, pericarditis, increasing pericardial effusion (Figure 1), and cardiogenic shock. He underwent intra-aortic balloon pump placement with no improvement in hemodynamics and subsequently an Impella 5.5 was placed. On post MI Day 3, he underwent pericardial window in the setting of shock and increasing pericardial effusion. Intraoperative TEE showed signs of tamponade physiology (Figure 2). Repeat echocardiograms and CTA was unrevealing of a rupture. Post MI day 6, he had increasing output from the drains and increasing pericardial effusion with complete right ventricular collapse on bedside echocardiogram. Emergent mediastinal exploration revealed left ventricular (LV) free-wall rupture which was repaired with a bovine patch. Hemodynamics improved and goal directed medical therapy was started. Discussion: Free wall rupture is a rare complication post MI and is reported in only 0.01% of STEMI. It usually occurs within 1 week, majority occurring within 24 h of MI. Small LV wall rupture can be challenging to diagnose on cardiac imaging. This case emphasizes the importance of having a high index of suspicion for diagnosing free wall rupture in patients presenting with hemodynamically unstable pericardial effusion post STEMI. Prompt pericardiocentesis and surgical intervention lead to a good outcome.

Abstract 19071: An Agitated Young Heart: A Rare Presentation With a Favorable Outcome Under the Right Circumstances

Introduction: Commotio cordis (Latin: agitation of heart) is sudden death triggered by a blunt, often innocent-appearing blow to the chest. It is the third most common cause of sudden cardiac death (SCD) in young athletes, after hypertrophy cardiomyopathy, and coronary anomalies. Around 10-20 cases are added to the Commotio Cordis (CC) registry annually. Ventricular fibrillation seems to be the most common arrhythmia in commotio cordis in 40% of cases. Case Presentation: A 22-year-old male with no known medical illness presented after sudden cardiac arrest. According to a bystander, he fell to the ground and lost consciousness within a few seconds of being “elbowed in his chest” during a basketball game. EMS provided bag valve mask ventilation for respiratory distress but were unable to record the rhythm. On initial presentation to the emergency room, he was found to be in ventricular tachycardia (VT) with hemodynamic instability. He was cardioverted, and his VT deteriorated to ventricular fibrillation. He was intubated for airway protection, received two rounds of CPR and another 200 J defibrillation that restored his sinus rhythm with return ofspontaneous circulation (ROSC). Bedside echocardiogram revealed global hypokinesis with EF 30-35%. EKG showed marked ST elevation in AvR with deep ST depression in other leads. Code STEMI was activated, and an emergent coronary angiogram was done which revealed normal coronary arteries and anatomy. Subsequent EKG within an hour was essentially normal. A repeat echocardiogram on the next day showed an improved EF of 65%. Discussion: Commotio cordis is fatal, with only about 25% of the cases on CC registry resulting in survival. A chest blow must be confined to a small area of the precordium within a 20 msec window during upstroke of T wave that results in ventricular fibrillation. Sustained ventricular tachycardia is even rare, with only one case report found on literature review. It is likely that his VT favored a better prognosis.

Abstract 18104: The Unexpected Disaster: Unusual Form of Left Ventricular Rupture

Description: We present a 73-year-old female, who presented with NSTEMI. EKG showed ST depression in the inferior and anterior leads. Initial Troponin I was high (0.17 ng/mL). She received nitroglycerine with no relief of her pain, so she underwent an emergent left heart catheterization (LHC). The LHC showed two tandem 90% stenosis in the right coronary artery (RCA) and mild disease in the left anterior descending (LAD) and left circumflex (LCx) arteries. PCI to the RCA was successful. She was started on a high-intensity statin, carvedilol, dual antiplatelet therapy, and losartan. On the day after PCI, an echocardiogram showed preserved ejection fraction with no evidence of pericardial effusion. The patient was doing well until 2 days after the PCI when she was found obtunded and hypotensive. She received normal saline bolus, epinephrine, and norepinephrine, after which she improved. A bedside echocardiogram revealed evidence of pericardial effusion with tamponade physiology and a pericardial clot. The patient and her family declined further interventions and elected to proceed with comfort measures. Discussion: Mechanical complications of acute myocardial ischemia (AMI) have substantially decreased in numbers after the implication of early reperfusion therapies, but they remain fatal if not recognized early and treated. Free wall rupture (FWR) usually occurs in the first 7 days following an AMI, with an average of 2.6 days. FWR mostly happens after infarction of the LAD or LCx territories. In our case, there was no delay in reperfusion therapy and there was no evidence of infarction on the echocardiogram however the patient developed FWR as a complication and in a timeline earlier than average making this case unique.

FRI502 Myxedema Coma With An Unusual Pattern Of Thyroid Function Tests Due To Amiodarone-induced Hypothyroidism

Abstract Disclosure: S. Nguyen: None. B. Force: None. R. Schneider Aguirre: None. Introduction: Myxedema coma is an endocrine emergency characterized by severe hypothyroidism resulting in altered mental status or coma, hypothermia, cardiovascular compromise, pulmonary edema or pleural effusions, and/or gastrointestinal hypomotility, classically in the context of an elevated TSH and low thyroxine levels. Amiodarone use is associated with alteration of thyroid function tests and could cloud the laboratory presentation of myxedema coma. Here we present a case of myxedema coma in a patient with amiodarone-induced hypothyroidism with an elevated free T4 (FT4) and low total T3 (TT3). Clinical Case: A 64-year-old female with a history of chronic systolic heart failure, persistent atrial flutter treated with amiodarone, cerebrovascular accident, hypertension, chronic kidney disease stage 4, but not hypothyroidism, presented with constipation, confusion and lethargy worsening over 3 days. On initial evaluation, she was minimally responsive, hypothermic to 95.6 °F and bradycardic to low 50s. She was intubated for airway protection and vasopressors were started due to concern for cardiogenic shock. Exam was notable for coarse facial features, edema and cold extremities. A bedside echocardiogram showed reduced cardiac function from baseline. Her TSH was 40.65 uIU/mL (RR, 0.45-5.33 uIU/mL), FT4 1.79 ng/dL (RR 0.64-1.42 ng/dL), total T4 14.30 mcg/dL (RR 6.09-12.23 mcg/dL), TT3 70 ng/dL (RR 87-178 70 ng/dL). Sodium was 135 mmol/L (RR 136-145 mmol/L), serum glucose was 42 mg/dL, (RR 70-110 mg/dL), and eGFR was 18 mL/min/1.73 m2 (baseline eGFR 28 mL/min/1.73 m2). Evaluations for myocardial infarction and infectious etiology were initiated and ultimately negative. While elevated FT4 is not characteristic of myxedema coma, the overall constellation of stupor, constipation, bradycardia, hyponatremia, hypoglycemia, decreased eGFR and decreased cardiac function, in the setting of an elevated TSH and low TT3, made the diagnosis of myxedema coma extremely likely. The patient was started on levothyroxine 200 mcg IV daily and hydrocortisone 100 mg IV every 8 hours. After 16-20 hours on this regimen, the patient was weaned off sedation and vasopressors, extubated, and recovered baseline mental status. Hydrocortisone was stopped and on day 3 of hospitalization, she was transitioned to oral levothyroxine 88 mcg daily. Due to premature ventricular contractions her dose was decreased to 50 mcg orally daily five days after her initial presentation to the hospital. During this time, the TSH decreased to 3.59 uIU/mL and the FT4 rose to 2.83 ng/dL. Conclusion: We conclude that in patients treated with amiodarone, myxedema coma can still occur even if T4 levels are normal or elevated, likely due to decreased T4 to T3 conversion. In these cases, elevated TSH and a clinical picture consistent with severe hypothyroidism are more reliable indicators if the (free) T4 levels are unexpectedly elevated. Presentation: Friday, June 16, 2023

Acute lymphocytic myocarditis presenting as complete heart block in an adult: a case report

BackgroundComplete heart block (CHB) as a first presentation of acute viral myocarditis is a rare occurrence associated with increased morbidity and mortality. In such cases, an endomyocardial biopsy is recommended to make a clear histological diagnosis aiding to differentiate from other possible conditions such as sarcoiditic myocarditis, giant cell myocarditis, and eosinophilic myocarditis. Insertion of a permanent pacemaker may be considered on a case-to-case basis.Case presentationA previously healthy 21-year-old female presented to the emergency department after having suffered two episodes of syncope on a background of a few days’ history of myalgias, chills, and rigors. Electrocardiogram showed high-grade Mobitz II block with intermittent periods of CHB. A bedside echocardiogram upon admission demonstrated normal biventricular systolic function. Given the patient’s unstable haemodynamic status and lack of obvious reversible causes for the CHB, a permanent dual-chamber pacemaker was inserted urgently. Initial blood investigations indicated an ongoing inflammatory process highlighting the possibility of myocarditis as a cause of the CHB. Therefore, a troponin level was taken and was noted to be elevated confirming the suspicion of myocarditis. The left ventricular ejection fraction (LVEF) decreased over the following days to approximately 20%, clinically resulting in pulmonary oedema and acute shortness of breath. The patient required aggressive intravenous diuresis and anti-heart failure medication. An endomyocardial biopsy (EMB) confirmed the diagnosis of lymphocytic myocarditis. The patient’s condition improved secondary to an improvement in LVEF and resolution of the heart block. A cardiac magnetic resonance (CMR) imaging performed 6 weeks from admission reported an improved LVEF of 51% with no late gadolinium enhancement (LGE). Based on the reassuring CMR findings and the resolution of CHB on follow-up pacemaker checks, it was deemed safe to explant the pacemaker.ConclusionsAcute myocarditis may be complicated with high-degree AV block and cardiogenic shock necessitating close observation in a critical care unit. A permanent pacemaker may provide atrio-ventricular synchrony which helps stabilise the patient’s condition and protect from a prolonged period of heart block. Early myocardial fibrosis on EMB and degree of LGE on CMR are indicators of persistent atrioventricular block. Guideline-directed treatment of heart failure is essential.

Cardiac Tamponade as the Cause of Pulmonary Edema: Case Report

Introduction: Cardiac tamponade is an emergency syndrome that requires fast diagnosis and treatment; otherwise patient follows obstructive shock and cardiac arrest. Case report: A 70-year-old female was brought to the emergency department with hypoxemia. She had a history of progressive dyspnea over the past three weeks. Past medical history includes smoking. On physical examination: tachypnea, hypoxemia (SaO2 89%), jugular venous distention, arterial pressure 220/100 mmHg, heart rate rhythmic of 82 bpm. On pulmonary auscultation: diffuse and bilateral crackles. Lung ultrasound showed a bilateral B line and the echocardiogram demonstrated a pericardial effusion with signs of tamponade. A pericardiocentesis evacuated 620 ml of hemorrhagic fluid and the patient was transferred to the intensive care unit, hemodynamically stable, with SaO2 95%. At the ICU the echocardiogram, showed resolution of the cardiac tamponade and a tumor adhered to the lateral wall of the left ventricle. Chest CT demonstrated: a left lung tumor, infiltrating the pericardial sac. A pericardium biopsy demonstrated undifferentiated carcinoma. Discussion: Cardiac tamponade diagnosis requires a high level of suspicion. Respiratory failure, chest pain, and shock, observed in cardiac tamponade, are also present in different diseases. The most common finding of cardiac tamponade is dyspnea (78% of cases). Our patient had dyspnea due to pulmonary edema, secondary to left ventricle diastolic dysfunction caused by the tamponade. A bedside echocardiogram made the diagnosis of cardiac tamponade and guided the effective pericardiocentesis. Conclusion: Cardiac tamponade must be suspected in all cases of acute dyspnea. Echocardiogram is the method of choice for the diagnosis and for guiding the pericardiocentesis.

Takotsubo cardiomyopathy following blunt trauma: Early recognition and diagnosis

Takotsubo Cardiomyopathy (TTC) is characterized by reversible left ventricular apical ballooning in the absence of angiographically significant coronary artery disease. While TTC is usually preceded by an emotionally stressful event, physical trauma has been documented as a precipitating incident as well.An 82-year-old female with no past medical history, presented to the emergency department following a motor vehicle collision. Trauma workup was significant for an ulnar fracture, elevated cardiac enzymes, and ST-segment changes. Bedside echocardiogram revealed apical ballooning. She underwent cardiac catheterization, which failed to demonstrate significant coronary artery disease. The patient developed cardiogenic shock and required temporary vasopressor support after failing a trial of intra-aortic balloon pump.Takotsubo Cardiomyopathy is a rare complication of trauma, which presents with signs and symptoms similar to acute coronary syndrome (ACS) but without evidence of obstructive coronary artery disease. Following trauma, signs of ACS in elderly women should raise provider's suspicion for TTC and prompting bedside echocardiography, which can assist with early diagnosis.

Point-of-Care Ultrasound of Post-acute COVID-19 Syndrome: A Prospective Cohort Study.

Introduction Acute COVID-19 patients can suffer from chronic symptoms known as post-acute sequelae of SARS-CoV-2 infection (PASC). Point-of-care ultrasound (POCUS) is established in acute COVID, but its utility in PASC is unclear. We sought to determine the incidence of cardiac and pulmonary abnormalities with POCUS in patients with PASC in a COVID-19 recovery clinic. Methods This prospective cohort study included adults (>18 years old) presenting with cardiopulmonary symptoms to the COVID-19 recovery clinic. A lung ultrasound and standard bedside echocardiogram were performed by ultrasound-trained physicians. Images were interpreted in real time by the performing sonographer and independently by a blinded ultrasound faculty member. Discrepancies in interpretation were addressed by consensus review. A modified Soldati score was calculated by the sum of the scores in each of the 12 lung zones, with each zone score ranging from 0 to 3 (maximum score of 36). The score was then compared to clinical outcomes and outpatient testing. Results Between April and July 2021, 41 patients received POCUS examinations, with 24 of those included in the study. In all, 15 out of 24 (62.5%) had a normal lung ultrasound. Of the nine subjects with lung abnormalities, the median modified Soldati score was 2. Three patients had trivial pericardial effusions, and all had normal left and right ventricular size and function. Conclusion The majority (62.5%) of patients presenting to the PASC clinic had a normal pulmonary ultrasound, and the vast majority (87.5%) had normal cardiac ultrasounds. These findings suggest that cardiopulmonary symptoms in PASC may be from etiologies not well evaluated by POCUS.

Unknown rheumatic cardiac disease as cause of acute onset post-partum dyspnea: a case report

BackgroundAcute post-partum dyspnea configures an obstetric challenge with multiple differential diagnosis.Case presentationWe present a case of a previous healthy woman with preeclampsia who developed severe dyspnea 30 h after delivery. She complained of cough, orthopnea, and bilateral lower extremities oedema. She denied headaches, blurry vision, nausea, vomiting, fever or chills. Auscultation revealed a diastolic murmur, and was compatible with pulmonary oedema. A timely bedside echocardiogram showed moderate dilated left atrium with severe mitral insufficiency suggestive of an unknown rheumatic disease. She was managed with noninvasive ventilation, loop diuretics, vasodilators, thromboprophylaxis, head-end elevation, and fluid restriction with progressive improving.ConclusionsHemodynamic changes in pregnant patients with previously silent cardiac disease may pose a challenge and cause post-partum dyspnea. This scenario requires a timely and multidisciplinary approach.

P71: Use of Veno-Arterial Extracorporeal Membrane Oxygenation and Impella for Cardiogenic Shock due to Cocaine Abuse

Background: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and Impella left ventricular assist device individually offer cardiovascular support for cardiogenic shock patients. Each modality has its own benefits and downfalls. We present a case in which a patient developed cocaine-induced coronary vasoconstriction resulting in cardiogenic shock with rapid systemic decompensation. We employed VA-ECMO and subsequent Impella to recover the patient. Methods: A 26-year-old male with a history of Graves’ Disease and chronic cocaine abuse presented to the ED with chest pain following cocaine ingestion. EKG showed sinus tachycardia and ST-elevations throughout, suspicious of coronary vasospasm. Labs showed an acute kidney injury as well as shock liver. Bedside echocardiogram (ECHO) revealed a severely depressed left ventricular ejection fraction (LVEF) of <10%. He was hemodynamically unstable for coronary catheterization and was emergently cannulated for VA-ECMO via the right femoral artery and left femoral vein. After we gained stability and slowly weaned the inotropic support. A follow-up ECHO revealed a dilated left ventricle and biventricular failure. With better hemodynamics, we did a catheterization showing coronary vasoconstriction, “clamping down” of distal vessels. (Figure 1) Due to the left ventricular dilation and its poor contractility, we decided to place an Impella. Results: The patient was supported on VA ECMO for 4 days, at which his LVEF recovered to 30-35%. The Impella device remained for an additional 3 days as his labs and hemodynamics improved. His LVEF at Impella removal was 40%. The patient was discharged in 14 days with a normal LVEF. Conclusion: One of the major downfalls of VA-ECMO is the lack of left ventricular unloading resulting in increased afterload and hindering recovery. An Impella can be used to help vent the left ventricle. This combination has been shown in several studies to improve outcomes in patients with acute coronary syndrome. The technique was employed with successful cardiac recovery in a patient who developed cardiogenic shock from coronary vasospasm from cocaine use.Figure 1. Coronary angiography showing coronary vasoconstriction due to cocaine use

P256 AN UNUSUAL CASE OF PACEMAKER MALFUNCTION WITH NON COMMON ELCTROCARDIOGRAPHIC PRESENTATION AND UNEXPECTED ECHOCARDIOGRAPHIC FINDING

Abstract This clinical case shows the diagnostic challenge and the management of a 79 y–o male with recent hospitalization for infero–lateral STEMI undergoing primary PCI of Right Coronary Artery with 2 DES and following DDDR MRI PM (pacemaker) implantation due to the development of persistent 2:1 Atrio–Ventricular Block. One month later, admission at Emergency Department for syncope. Normal parameters were found at laboratory analyses. The electro–stimulator activity evaluation showed a PM malfunction with ventricular capture failure. Thus, the increase of PM output up to electric ventricular capture (8 Volt/120 msec) was performed, but the following Electrocardiogram showed a PM–induced rhythm with RBBB–morphology. Then, the bedside Echocardiogram showed an apparent presence of a linear hyper–echogenic image into left ventricle with no inter–ventricular septal defect neither inter–ventricular shunt, inter–atrial septal hypermobility with no evident inter–atrial shunt at rest; while a chest Radiography identified the atrial and ventricular leads with no accurate individuation of their position. The patient was admitted in Intensive Cardiac Care Unit with confirmation of intermittent failure to ventricular capture and RBBB–morphology during PM–induced rhythm at telemetry monitoring. Due to Electrocardiographic and Echocardiographic findings, a strong suspect of abnormal position of the ventricular lead into left ventricle through a possible PFO has been raised. A chest Computed Tomography was performed confirming the anomalous position of the ventricular lead: it reached the left atrium through an inter–atrial defect/patent foramen ovale (PFO), then crossing the mitral valve up to left ventricle. The PM–lead repositioning was scheduled two days after. After positioning of temporary stimulator lead in right ventricle, the ventricular lead has been withdrawn from left–side chambers and positioned into septal–apical right ventricle; furthermore, the position of right atrial lead has been optimized (because of frequent spontaneous passage to the left atrium through the PFO, during manual maneuvers) thus obtaining good stability of the device. During the following days, the telemetry monitoring showed a PM–induced rhythm, without capture nor sensing failure. The chest Radiography confirmed the correct position of leads and the pre–discharge Echocardiography showed a LVEF 57% with no valvular pathology and with atrial and ventricular leads into right–side chambers.

P50 ODD CONNECTIONS

Abstract A 40 yo man was admitted to the ER due to typical oppressive chest pain at rest; he had no previous medical history and he denied any cardiovascular risk factor, including family history of cardiac disease. He was actually a sportsman, practicing martial arts. The basal ECG showed sinus rhythm, and an early repolarization pattern with no pathological features. Physical examination revealed a continuous cardiac murmur (2/6) along the sternal border and no other pathological signs. Three consecutive HsTnI determinations resulted negative. He was evaluated by the cardiologist, and a bedside echocardiogram resulted unremarkable. Due to the typical characteristics of the symptoms, an exercise ECG was performed, and the results were suspicious for inducible ischemia at high workloads. He was then admitted to our Cardiology ward, where he underwent a coronary angiography that showed a really surprising and unexpected anatomy: numerous coronary fistulas arising from various tracts (mid–LAD, intermediate coronary artery, conal branch of RCA, and distal Cx). A CT coronary angiogram was then performed, showing some ectasic vascular malformations between different coronary arteries, between coronaries and the pulmonary artery, and also a vascular anomaly connecting a bronchial artery with the right pulmonary artery. We subsequently performed a full body CT angiogram and a cerebral MR angiography, that excluded the presence of extrathoracic arteriovenous malformations. This case shows an extremely rare coronary congenital anomaly (accounting for 0.08–0.4% of all congenital heart disease), that generally goes underdetected in the first decades of life of these subjects. In this case, the typical anginal symptoms (probably due to coronary “steal” mechanism) arose suspicion that lead to the, albeit least expected, odd diagnosis. The treatment of symptomatic coronary fistulas is percutaneous/surgical closure. The patient was referred to our Tertiary Centre GUCH department, where a multidisciplinary discussion will decide the best therapeutic strategy.

The additive role of cardiac CT in a patient with cardiogenic shock and suspected mechanical complication of myocardial infarction.

A 69-year-old woman with previous hypertension and type-2 diabetes was admitted to the emergency department with syncope, referring continuous chest pain in the last 4 days. At hospital admission, the patient was in cardiogenic shock. The initial electrocardiogram showed Q waves in the anterior wall and ST-segment elevation on the anterior, lateral, and inferior walls. A bedside echocardiogram was immediately performed (panels A and B; Supplementary data online, Video S1) which showed a dilated left ventricle (LV) with severe LV systolic dysfunction and akynesia of the mid-apical segments of all ventricular walls. The patient had pericardial effusion (PE) with images suggesting clots near to the right ventricle free wall, with tamponade criteria. Although no rupture of the LV wall was clearly visible on echocardiogram, there was a high clinical suspicion of this complication. Cardiac computed tomography (CT) angiography confirmed myocardial rupture at the distal segment of the anterior wall and a mild circumferential PE, with a fluid density suggestive of haematic content (panels C, D, and E; Supplementary data online, Video S2). The patient underwent emergent surgery (panel F; Supplementary data online, Video S3) to correct the LV free wall rupture.

AI-ENABLED ASSESSMENT OF CARDIAC FUNCTION AND VIDEO QUALITY IN EMERGENCY DEPARTMENT POINT-OF-CARE ECHOCARDIOGRAMS

BackgroundThe adoption of point-of-care ultrasound (POCUS) has greatly improved the ability to rapidly evaluate unstable emergency department (ED) patients at the bedside. One major use of POCUS is to obtain echocardiograms to assess cardiac function. ObjectivesWe developed EchoNet-POCUS, a novel deep learning system, to aid emergency physicians (EPs) in interpreting POCUS echocardiograms and to reduce operator-to-operator variability. MethodsWe collected a new dataset of POCUS echocardiogram videos obtained in the ED by EPs and annotated the cardiac function and quality of each video. Using this dataset, we train EchoNet-POCUS to evaluate both cardiac function and video quality in POCUS echocardiograms. ResultsEchoNet-POCUS achieves an area under the receiver operating characteristic curve (AUROC) of 0.92 (0.89–0.94) for predicting whether cardiac function is abnormal and an AUROC of 0.81 (0.78–0.85) for predicting video quality. ConclusionsEchoNet-POCUS can be applied to bedside echocardiogram videos in real time using commodity hardware, as we demonstrate in a prospective pilot study.

Transient Right Bundle Branch Block with S1Q3T3 Pattern in Pulmonary Embolism

A 69-year-old woman with hypertension, hyperlipidemia, sleep apnea, gastroesophageal reflux disease, and recent knee replacement was brought to the emergency room (ER) for syncope. She had her physiotherapy session earlier in the day and became symptomatic with dizziness, shortness of breath and had loss of consciousness. In the ER, systolic blood pressure (SBP) was noted to be 90 mmHg and an oxygen saturation (O2 sat) of 80% on room air. Patient received fluid bolus with improvement of SBP to 110 mmHg. O2 sat improved to 99% with 10 L of oxygen. A bedside echocardiogram showed right ventricular (RV) distension. A Computerized Tomographic Angiogram (CTA) of the chest showed bilateral main stem pulmonary emboli (PE) with signs of RV strain. Initially EKG showed sinus tachycardia, right bundle branch block, and a S1Q3T3 pattern which resolved rapidly the next day. Patient was admitted, remained hemodynamically stable, and was treated with full dose of Enoxaparin subcutaneously. A follow up EKG was performed the next day, which showed complete resolution of initial findings. Follow up echocardiogram also showed rapid resolution of RV strain and complete restoration of RV size and function. Patient was eventually discharged home on full dose apixaban.

285 BIVENTRICULAR TAKO-TSUBOSYNDROME ASSOCIATED WITH SYNCOPE AND UNCONSCIOUSNESS

Abstract A 58-years old woman came to the emergency department due to syncope; she had been found lying on the ground in her residence. At the admission the patient was unconscious but had preserved blood pressure 120/80 mmHg. CT brain scan was negative for hemorrhage. Admission ECG showed a 52 b/m sinus bradycardia, elevated antero-septal ST segment and prolonged QT interval. Diagnosis of antero-septal STEMI was made and a coronary angiogram performed via right femoral access showed mild atheromasia in the absence of angiographically significant lesions. Bedside echocardiogram showed severe left ventricular dysfunction (LVEF 35%) with akinesia of apical and mid-ventricular segments. The right ventricle presented a marked hypocontractility of the apical region and a preserved kinetics of the basal portion (TAPSE 22 mm). There was also a moderate mitral regurgitation and a mild tricuspid regurgitation with a sPAP of 50 mmHg (40+10). On blood sampling, high-sensitivity troponin was slightly elevated (3950 pg/ml) and marked hyponatriemia (117 mmol/l) and slight hypokalemia (3.1 mmol/l) were noted. The echocardiogram on the third day showed an improvement in global and segmental kinetics of left ventricle with an estimated EF of 45% and persistence of a mild hypocontractility of the apex of right ventricle. During her hospital stay, her cognitive state gradually improved and she remained asymptomatic without evidence of arrhythmic events on monitoring. The ECG evolved on days with normalization of the ST-T tract, negative T wave in the anterior region and prolonged QTc interval. The pre-discharge echocardiogram showed a recovery of biventricular kinetics with an estimated EF of 50%. The presence of a transient abnormality in biventricular wall motion beyond a single epicardial coronary artery perfusion territory with new electrocardiographic change met the diagnostic criteria of Tako-tsubo Syndrome defined by Mayo Clinic criteria. The electrocardiogram on the day of discharge showed a 55 b/m sinus bradycardia with a negative T wave from V1 to V4. Tako-tsubo syndrome (TTS) is an acute and reversible left ventricular dysfunction that improves spontaneously within days or weeks and is often preceded by emotional or physical stress. Biventricular involvement in TTS is typically identified on imaging studies such as echocardiography and MRI. TTS with RV involvement is associated with a higher rate of in-hospital mortality and long-term adverse clinical events than isolated LV TTS. In our clinical case, biventricular involvement was associated with a severe clinical presentation (syncope and unconsciousness). This case shows that biventricular Tako-tsubo is a clinical scenario that requires intensive care monitoring and strict cardiological evaluation.