Pulsus Paradoxus Research Articles

Use of the pleth variability index in children with obstructive respiratory disease

IntroductionThe phenomenon of pulsus paradoxus (PP) develops at varying rates in relation to the severity of the disease in obstructive respiratory tract disease. The Pleth Variability Index (PVI) is the measurement value of perfusion index changes that occur with ventilation, which are determined during at least one respiratory cycle. Therefore, noninvasive measurement of PVI can help in the measurement of PP. The current study aims to determine the role of PVI measurements before and after bronchodilator therapy during admission to the hospital in children with obstructive respiratory tract disease. MethodsAge, gender, Pulmonary Index Score (PIS), and PVI data of patients aged 2–18 years who applied to the pediatric emergency department with signs of obstructive respiratory tract disease were recorded in triage. The PVI and PIS scores of the patients, who were divided into three groups according to their clinical severity scores, were recorded before and after bronchodilator treatment, and they were compared to the PVI values according to the disposition results. ResultsA total of 133 patients were included in this prospective, single-center study. The PVI values before and after treatment were significantly higher in patients with severe disease compared to the mild and moderate groups (p < 0.001). Post-treatment PVI values were significantly lower than pre-treatment values in all clinical severity groups (p < 0.001). While a total of 95 (71.43%) patients were discharged from the emergency department, 31 (23.31%) patients were admitted to the relevant department, and seven (5.26%) patients were admitted to the pediatric intensive care unit. The PVI values before and after treatment were significantly higher in the hospitalized group compared to the group discharged from the emergency department (p < 0.001). The areas under the ROCs were 0.940, 0.865, and 0.843 for the PVI measurements in patients with severe disease, moderate disease, and hospitalization (p< 0.001). ConclusionsAutomated PVI measurement can be used as a noninvasive, rapid, and objective tool in the emergency department triage of patients admitted to the pediatric emergency department with signs of asthma attack or reactive respiratory tract disease.

Cardiac Tamponade in Eisenmenger Syndrome: A Diagnosing Complexity: Case Report

Cardiac tamponade is a form of obstructive shock with clinical manifestations consistent with a low cardiac output and high central venous pressure. Features of a low cardiac output include low mean arterial pressure, cold peripheries and signs of poor end-organ perfusion. Characteristically, palpating the pulse reveals an apparent variation in pulse volume because of pulsus paradoxus. Jugular venous pressure is typically increased, with distended neck veins apparent. Sympathetic tone is increased in an attempt to compensate for the low cardiac output and manifests as tachycardia, diaphoresis, anxiety [1] and poor distal perfusion determining the need for emergent Pericardiocentesis. We report a case where an hemodynamically significant pericardial effusion with indication of pericardiocentesis had presented without classic signs of tamponade. It is an unusual and rare case of large pericardial effusion in the setting of Eisenmenger syndrome where only clinical signs as worsening hypoxia and cyanosis due to the right to left shunt was the warning sign of cardiac tamponade requiring pericardiocentesis.

Abstract 17237: A Pair Of Diaphragm-Crossed Organs: A Pancreatico-Pericardial Fistula

Introduction: Pseudocysts are a known complication of chronic pancreatitis, occurring in 30-40% of patients. They form when disruption of the pancreatic duct system creates fluid-filled pockets with high concentrations of digestive enzymes. Leakage of these enzymes can create pancreatic fistulas. Here, we present a case of an unusual fistula that occurred in an immunocompromised individual. Case Description: A 34-year-old man with a history of Acquired Immunodeficiency Syndrome, alcohol use disorder, and chronic pancreatitis who had recently recovered from acute pancreatitis complicated by pericardial effusion was readmitted with worsening pleuritic chest pain and shortness of breath. He was hemodynamically stable with a normal cardiopulmonary exam without jugular venous distention or pulsus paradoxus. Labs were at his baseline other than an elevated d-dimer level. Computed tomography scan revealed a large, loculated pericardial effusion with a fistula extending through the diaphragm to a large peripancreatic pseudocyst. Gastroenterology performed pancreatic ductal stenting via endoscopic retrograde cholangiopancreatography and Interventional Radiology placed a percutaneous drainage catheter to facilitate resolution of the pseudocyst. Discussion: A pancreatico-pericardial fistula is a very rare complication of chronic pancreatitis. A 2016 review detailed only fifteen cases over a 40-year span with surgical management providing the best outcomes. Given this patient’s immunocompromise and malnutrition surgery was not offered, but endoscopic stenting and percutaneous drainage allowed for successful resolution of his fistula.

Abstract 12913: Under Pressure: An Unusual Case of Pulmonary Hypertension and Pericardial Effusion

A 50-year-old male smoker with hypertension presented with subacute bilateral leg swelling, weight gain, and dyspnea. Exam revealed tachycardia, jugular venous distention, peripheral edema, diminished breath sounds, and pulsus paradoxus. Labs were notable for elevated creatinine and leukocytosis. ECG showed sinus tachycardia and low voltages. CXR showed left hemithorax opacification. TTE revealed normal LV function, septal flattening, severely dilated RV with reduced function, RVSP 81 mmHg, and a large pericardial effusion with exaggerated respirophasic variation in mitral inflow but no chamber collapse. The elevated RVSP with RV failure raised concern for acute pulmonary embolism (PE). CT chest excluded PE but revealed a large mediastinal mass compressing both pulmonary arteries (PA) and large left pleural effusion. Pulmonary angiogram demonstrated a totally occluded left PA and severe stenosis of the right PA. Right heart catheterization showed RAP 24, RV 83/21, PA 84/29 (mean 53), intrapericardial pressure 15 mmHg, and low cardiac index (1.6 L/min/m2). Pericardiocentesis was performed with close monitoring by PA catheter. Removal of 500cc fluid was well tolerated with stable hemodynamics, cardiac output, and intracardiac pressures. Pericardial fluid cytology and lymph node biopsy demonstrated small cell lung cancer. Cautious diuresis was initiated. After one cycle of chemotherapy, repeat CT chest showed reduced extrinsic compression of the right PA with improved lung perfusion. Repeat TTE showed dramatic improvement with normal RV size and function, RVSP 22 mmHg, and trivial pericardial effusion. Pericardial effusion in the setting of severe PH is associated with poor outcomes and presents both diagnostic and therapeutic challenges. Classic findings of tamponade (e.g. right sided chamber collapse) may be masked by elevated right heart pressures. Compression of the PA by a mediastinal mass is an unusual cause of PH and right heart failure that can mimic acute PE. This rare clinical scenario presents the following challenges: (1) diuresis may precipitate tamponade, (2) pericardiocentesis may enable an already enlarged RV to acutely dilate and thus worsen RV failure, and (3) there is uncertainty regarding the role for PA stenting.

Abstract 9307: A Heart of Gold: A Case Report of Massive Pericardial Effusion Secondary to Cholesterol Pericarditis

A case of rare cholesterol pericarditis that developed over 12 years resulting in a massive pericardial effusion containing cholesterol crystals is described. A 41-year-old homeless man with history of polysubstance intravenous drug abuse and upper respiratory and soft-tissue infections presented with evidence of recurrent left lower extremity cellulitis, mild shortness of breath, and palpitations. Physical exam demonstrated soft-tissue infection, marked tachycardia and distant heart sounds on auscultation, and jugular venous distention. Unexpectedly, pulse-oximetry plethysmographic waveforms revealed pronounced respirophasic variability and pulsus paradoxus of 14 mmHg. Electrocardiogram demonstrated low voltage and electrical alternans. A transthoracic echocardiogram revealed a large pericardial effusion and findings consistent with tamponade physiology, such as elevated respiratory variation in mitral inflow velocity. Emergent pericardiocentesis yielded 3.6 L of fluid characterized by glittering, gold paint-like appearance and a cell count predominated by macrophages, leading to a provisional diagnosis of cholesterol pericarditis. This was confirmed by polarized light microscopy demonstrating cholesterol crystals. Retrospective review of prior emergency department visits revealed a 12-year development of the effusion, beginning with symptoms, imaging, and labs consistent with a presumably instigating viral respiratory illness. Over time, progressive enlargement and evidence of chronic pericarditis were demonstrated by chest x-ray and electrocardiography, while the effusion remained undiagnosed. Following improvement in his symptoms after pericardiocentesis, the patient deferred pericardial window and definitive surgical management with pericardiectomy. Given his high risk for recurrent cardiac tamponade, he was given clear return precautions and is now followed on an outpatient basis. The diverse etiologies of cholesterol pericarditis, such as hypothyroidism, tuberculosis, and rheumatoid arthritis, that guided the workup for this patient, and the pathophysiology of this disease and its treatment options, are reviewed.

TO DRAIN OR NOT TO DRAIN: A THERAPEUTIC CONUNDRUM IN A PATIENT WITH PERICARDIAL TAMPONADE AND EISENMENGER SYNDROME

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: PAH is diagnosed when mean pulmonary artery pressure is greater or equal to 20 mmHg at rest with a pulmonary vascular resistance =3 Wood units. In regions without endemic schistosomiasis, it is commonly idiopathic (1). Eisenmenger syndrome (ES) is the most advanced form of pulmonary arterial hypertension (PAH) and is associated with several congenital heart defects such as ASDS, VSDS etc. CASE PRESENTATION: We present the case of a 30-year-old patient with a past medical history of Trisomy-21, unrestricted ventricular septal defect (VSD) complicated by Eisenmenger Syndrome, PAH (On Treprostinil and Bosentan), chronic hypoxia and Hashimoto's Thyroiditis, who presented from his group home for acute on chronic shortness of breath and fever. Initially, he was hypoxic and hypotensive with signs of severe volume overload on physical exam. Oxygen saturations improved mildly on high flow nasal cannula (HFNC). CT chest and bedside echocardiogram showed a massive pericardial effusion (4.5 cm at the largest point) with tamponade physiology, and pulsus paradoxus (Figure 1,2,3). He was started on vasopressors, inotropes, intravenous prostacyclin and inhaled epoprostenol. Extracorporeal membrane oxygen (ECMO) was planned to stabilize him and drain the effusion, but the family refused ECMO. A Swanz Ganz catheter was placed under fluoroscopic guidance to help guide management but it crossed the VSD and inadvertently ended up in the aorta after which it was removed. After multiple discussions with adult congenital heart disease experts, it was decided that draining the pericardial effusion was not an option given the concern for acute right ventricular failure which could precipitate hemodynamic collapse and cardiac arrest. Another concern was bleeding complications especially bleeding into the pericardial cavity from inadvertently puncturing the multiple collateral vessels that such patients develop. The patient gradually developed increasing vasopressor requirements and eventually passed away. DISCUSSION: A pericardial effusion develops when fluid accumulates between the two layers of pericardium. In PAH, it may develop due to elevated right atrial pressures or underlying connective tissue disease. Its presence in PAH is associated with a significantly increased risk of death and the decision to drain such an effusion remains highly controversial. Multiple studies have reported dismal prognosis of patients who have had such effusions drained (2). The Euro heart survey reported that mortality was particularly high in patients with Eisenmenger's, and they had an increased frequency of major bleeding events as well (2). CONCLUSIONS: Pericardial effusion drainage in patients with pulmonary arterial hypertension is controversial and is associated with poor outcomes. Mortality is particularly high in patients with Eisenmenger's, and a multidisciplinary approach should be utilized to manage such patients. REFERENCE #1: Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic definitions and updated clinical classification of pulmonary hypertension. Eur Respir J. 2019;53(1):1801913. REFERENCE #2: Engelfriet PM, Duffels MG, Möller T, et al. Pulmonary arterial hypertension in adults born with a heart septal defect: the Euro Heart Survey on adult congenital heart disease. Heart. 2007;93(6):682-687. DISCLOSURES: No relevant relationships by Saad Farooq, source=Web Response No relevant relationships by ELLIOT SULTANIK, source=Web Response No relevant relationships by Guy Weigold, source=Web Response No relevant relationships by Omar Yacob, source=Web Response

Electrocardiogram Findings Associated With Malignant Pericardial Effusion and Cardiac Tamponade.

Electrocardiogram Findings Associated With Malignant Pericardial Effusion and Cardiac Tamponade.

Resuscitative transesophageal echocardiography in the diagnosis of post-CABG loculated pericardial clot causing cardiac tamponade

BackgroundPericardial effusion is a known complication of post-open cardiac surgery which can progress to life-threatening cardiac tamponade. Classical signs of tamponade such as hypotension and pulsus paradoxus are often absent. Diagnosing acute cardiac tamponade with transthoracic echocardiography (TTE) can be challenging in post-cardiac surgical patients due to distorted anatomy and limited scanning windows by the presence of surgical dressings or scar. Additionally, this patient population is more likely to have a loculated pericardial effusion, or an effusion that is isoechoic in appearance secondary to clotted blood. These findings can be challenging to visualize with traditional TTE. Missed diagnosis of cardiac tamponade due to loculated pericardial clot can result in delayed diagnosis and clinical management.Case presentationWe report a case series that illustrates the diagnostic challenge and value of resuscitative transesophageal echocardiography (TEE) in the emergency department (ED) for the diagnosis of cardiac tamponade due to posterior loculated pericardial clot in post-surgical coronary artery bypass graft (CABG) patients.ConclusionsCardiac tamponade due to loculated posterior pericardial clot post-CABG requires prompt diagnosis and appropriate management to avoid the potential for hemodynamic instability. Transesophageal echocardiography allows a rapid diagnosis, early appropriate referral and an opportunity to institute appropriate therapeutic measures.

Clinical audit of the management of pericarditis in children in a Tertiary Referral University Hospital in Egypt

BackgroundGlobally, pericarditis is the commonest form of pericardial disease. Pediatric pericarditis has diverse etiologies and its available epidemiological data and management guidelines are sparse.ObjectiveTo evaluate the management of children with pericarditis attending Assiut University Children Hospital according to the European Society of Cardiology (ESC) guidelines (2015).Patients and methodsThis descriptive study was conducted at Assiut University Children Hospital, Assiut, Egypt, during the period of 1 year (from June 2017 to June 2018). During the study period, 30 children with pericarditis (due to different causes) were included (14 males and 16 females). Full history, cause of pericarditis, symptoms, and signs were taken. Some investigations, including laboratory and radiological were recorded. Therapy and medication and the outcome measures were assessed. In addition, the approach of doctors toward the application of the ESC guidelines was investigated.ResultsIdiopathic pericarditis was the most common cause of pericarditis (43.3%) followed by renal (20.0%), autoimmune (16.7%), tuberculosis (10.0%), and malignant (10.0%) causes. Chest pain (61–100%) followed by dyspnea (40.0%) was the most common presenting symptom. Tachycardia was a common sign in all cases, followed by muffled heart sound (in approximately two-thirds of cases), friction rub, jugular vein distention, and pulsus paradoxus, successively. Of the 30 included cases, 14 (46.6%) cases improved, nine (30.0%) cases got recurrent pericarditis, and seven (23.3%) cases died.ConclusionThe ESC guidelines (2015) help improve the management of pediatric pericarditis. It was followed by a reasonable percentage of our cases. It is strongly recommended for doctors to be trained to apply these guidelines. Future multicenter, long-term prospective studies are needed to develop therapeutic recommendations for pericarditis in pediatric patients in addition to understanding the pathophysiology for improving the outcome.

Oximetry‐detected pulsus paradoxus predicts asthma severity

Oximetry‐detected pulsus paradoxus predicts asthma severity

Effusive-constrictive cholesterol pericarditis: a case report.

BackgroundCholesterol pericarditis (CP) remains a rare pericardial disease characterized by chronic pericardial effusions with high cholesterol concentrations with or without the formation of cholesterol crystals. Effusions are often large and can cause ventricular compression and subsequent pericardial adhesion formation. CP can be idiopathic but has associations with rheumatoid arthritis (RA), tuberculosis and hypothyroidism.Case summaryWe present a case of a 72-year-old male with a background of seropositive RA with a finding of an incidental pericardial effusion on computed tomography thorax abdomen and pelvis. Transthoracic echocardiogram demonstrated a large effusion with echocardiographic features of tamponade. On review, he was breathless with a raised venous pressure, bilateral ankle oedema, and pulsus paradoxus was present. Pericardial drainage was performed with fluid analysis demonstrating a cholesterol concentration of 8.3 mmol/L and numerous cholesterol crystal formation. Interval imaging demonstrated recurrence of the effusion with pericardial thickening and progressive constriction. He remained asymptomatic and underwent a successful pericardial window. At present, he is under close clinical outpatient surveillance with symptoms guiding a future pericardiectomy if warranted.DiscussionCP can present as an emergent situation with signs and symptoms of acute heart failure with prompt pericardiocentesis required in cases of clinical tamponade. However, the disease course is often one of chronicity with relapsing large effusions that tend to recur following drainage, with the development of pericardial constriction necessitating pericardiectomy for definitive management.

Interstitial pneumonia with autoimmune features.

Cardiac tamponade is a medical emergency. This study was carried out to determine the etiologies of cardiac tamponade and review the management and outcomes. We retrospectively analysed case records of patients who underwent pericardiocentesis for cardiac tamponade during the two consecutive years (1 January 2018 to 31 December 2019) at Hospital Sultanah Nora Ismail, Batu Pahat, in Johor, Malaysia. There were ten patients (eight males, two females; age range 20 to 70 years old, mean age 36 years old) who underwent pericardiocentesis for cardiac tamponade during the said period. Malignancy (40%), tuberculosis (30%), idiopathic (20%), and bacterial (10%) were among the common causes of the pericardial effusion in this center. The commonest symptoms were breathlessness (90%), chest pain (60%), cough (50%), and unexplained fever (20%). Pulsus paradoxus was the most speciÿ c sign (100%) for the presence of echocardiographic feature of cardiac tamponade. Two of the patients with tuberculous pericarditis had retroviral disease; one patient had bacterial pericarditis due to salmonella typhi. This study has conÿ rmed that there are many etiologies and presentation of cardiac tamponade; clinicians should be alert as urgent pericardiocentesis is lifesaving.

A study of etiology, clinical characteristics, electrocardiographic and echocardiographic findings in patients with cardiac tamponade in a tertiary care hospital in Western Odisha

Background: Cardiac tamponade is a life-threatening condition characterized by elevated intracardiac pressure, limitation of diastolic filling, and reduction of cardiac output and mostly requires urgent therapeutic intervention. Pericardial disease in on the rise attributed to improved survival of malignancy, growing no of cardiac interventions, chronic kidney diseases with dialysis, advent of modern chemo-radiotherapy. Still, there are paucity of data on etiology, clinical characteristics, electrocardiogram (ECG) and echocardiographic features in patients with cardiac tamponade from Odisha. Aim of this study was to emphasize the etiology, clinical characteristics, electrocardiographic and echocardiographic features in patients with cardiac tamponade.Methods: A prospective observational study of 1-year duration was undertaken for patients with cardiac tamponade admitted at VIMSAR, a cardiology unit. Data on etiology, clinical characteristics, Echocardiography, ECG findings were documented. Echo guided pericardiocentesis followed culture, cytological and biochemical analysis done.Results: Most common symptom was dyspnoea (88%), clinical signs were tachypnoea (96%), raised jugular venous pulse (64%), tachycardia (84%), pulsus paradoxus (60%). Classical beck’s triad was seen in 42% cases. X-ray showed cardiomegaly (94%) &amp; pleural effusion (64%). Common ECG findings were sinus tachycardia (84%), low voltage QRS (68%) and electrical alternans (44%). Echocardiography showed 80% and 68% of patients had right atrium collapse and right ventricle collapse respectively. Both inferior vena cava plethora and transmitral flow variation were seen in 88% of cases. 96% had normal left ventricle function. 80% had large effusion. Pericardiocentesis yield was mostly in between 500-1000ml (mean 908 ml) with 72% with haemorrhagic aspirate. All malignancy cases and 76% tubercular cases had haemorrhagic effusion. Most common etiology was tubercular (50%), followed by malignancy (28%). 6% remained idiopathic. chronic kidney disease, systemic lupus erythematosus, post MI intervention, hypothyroid were some of the other causes.Conclusions: Initial assessment with investigation and careful follow-up can yield a causal diagnosis in most cases. Early diagnosis and intervention by pericardiocentesis can be lifesaving.

Abstract 13129: Chest Pain and Inflammation: A Story Where Hickam’s Dictum Prevailed

A 39-year-old male presented with a chief complaint of chest pain that worsened with deep breathing for one day. He was found to be tachycardic, with distant heart sounds and a skin nodule over his right upper extremity. ECG revealed diffuse ST elevations and PR segment depressions with TTE showing a small pericardial effusion. Troponin I was 8.98 ng/mL and NT-proBNP was 981 pg/mL. One day after admission, he developed respiratory distress, and repeat TTE showed a large pericardial effusion with collapse of the RV free wall during diastole with variation of mitral and tricuspid valve inflows consistent with tamponade. Pulsus paradoxus was 24 mmHg and he was taken for pericardiocentesis. Skin nodule biopsy revealed nodular and interstitial granulomatous dermatitis. Anti-nuclear antibody and double stranded DNA antibody were positive with pericardial fluid cytology showing acute inflammation with lupus erythematosus cells. Based upon this constellation of findings, he was diagnosed with systemic lupus erythematosus (SLE) myopericarditis, and started on colchicine and immunosuppression, with resolution of symptoms. One week into hospitalization, the chest pain recurred but was sharp and substernal, with a rising troponin from 1.23 ng/mL to 8.23 ng/mL. TTE showed depressed LVEF of 45% and RCA territory hypokinesis without effusion. CTA PE showed no evidence of thromboembolism and CT coronary demonstrated mural thickening of the mid LAD and aneurysmal dilation of the left main to the LAD and left circumflex bifurcation concerning for vasculitis. The mid RCA was occluded, and patient was taken to the cardiac catherization laboratory revealing thrombotic occlusion of the proximal-to-mid RCA. Despite serial balloon dilation, thrombotic occlusion persisted, Aspiration thrombectomy evacuated organized thrombus prior to deployment of two overlapping drug-eluting stents in the proximal-to-mid RCA, restoring flow. TTE prior to discharge showed normal LVEF and no effusion. This case illustrates various cardiac manifestations of SLE and the unusual dynamic nature of this patient’s multiple presentations of chest pain. Avoiding “diagnostic anchoring” is important to diagnosing and treating conditions such as SLE, that can affect the heart in multiple ways.

Abstract 13004: Spelunking for a Cause of Heart Failure: A Fungus Amongst Us

Two months prior to presenting to our facility, a 63-year-old man was diagnosed with acute pericarditis and treated with colchicine. His chest pain resolved, but he was readmitted a few weeks later with tamponade due to a large exudative pericardial effusion requiring percutaneous drainage. He was discharged on colchicine and furosemide; however, he presented to our institution two weeks later with persisting dyspnea and edema. His blood pressure was 114/84 mmHg without a pulsus paradoxus. Jugular venous pressure was 13 cm H 2 O with a prominent Kussmaul’s sign and 3+ bilateral leg edema. Further evaluation with a transthoracic echocardiogram, cardiac MRI and cardiac catheterization were all consistent with effusive-constrictive pericarditis (Fig A-F). 8-months prior to admission a mediastinal lymph node biopsy noted histoplasma. During admission, chronic histoplasmosis was suspected and a serum histoplasma antigen was reactive (1:256). He was initiated on 12 weeks of itraconazole; however, despite anti-inflammatory therapies, he had refractory congestion. Cardiothoracic surgery was consulted and he underwent pericardial stripping (Fig. G). Pericardial fungal cultures were negative and histopathology noted acute and chronic fibrinous pericarditis without fungal organisms (Fig. H-I). He had an uncomplicated recovery with symptom resolution. Histoplasma capsulatum is endemic to the United States and despite &gt;80% of individuals in endemic areas demonstrating exposure, cases of pericarditis, tamponade or pericardial constriction are rare. Pericardial inflammation likely reflects an autoimmune reaction to H. capsulatum rather than direct pericardial infection and may respond to anti-inflammatories. In sum, we describe a rare diagnosis of effusive-constrictive pericarditis secondary to chronic histoplasmosis. Our case highlights the salient findings of pericardial constriction and the continued importance of a detailed clinical history.

Massive pericardial effusion and cardiac tamponade revealed undiagnosed Turner syndrome: a case report

BackgroundPatients with Turner syndrome (TS) are prone to autoimmune disorders. Although most patients with TS are diagnosed at younger ages, delayed diagnosis is not rare.Case presentationA 31-year-old woman was presented with facial edema, chest tightness and dyspnea. She had primary amenorrhea. Physical examination revealed short stature, dry skin and coarse hair. Periorbital edema with puffy eyelids were also noticed with mild goiter. Bilateral cardiac enlargement, distant heart sounds and pulsus paradoxus, in combination with hepatomegaly and jugular venous distention were observed. Her hircus and pubic hair was absent. The development of her breast was at 1st tanner period and gynecological examination revealed infantile vulva. Echocardiography suggested massive pericardial effusion. She was diagnosed with cardiac tamponade based on low systolic pressure, decreased pulse pressure and pulsus paradoxus. Pericardiocentesis was performed. Thyroid function test and thyroid ultrasound indicated Hashimoto’s thyroiditis and severe hypothyroidism. Sex hormone test revealed hypergonadotropin hypogonadism. Further karyotyping revealed a karyotype of 45, X [21]/46, X, i(X) (q10) [29] and she was diagnosed with mosaic + variant type of TS. L-T4 supplement, estrogen therapy, and antiosteoporosis treatment was initiated. Euthyroidism and complete resolution of the pericardial effusion was obtained within 2 months. ConclusionHypothyroidism should be considered in the patients with pericardial effusion. The association between autoimmune thyroid diseases and TS should be kept in mind. Both congenital and acquired cardiovascular diseases should be screened in patients with TS.

ATRIAL FLUTTERS AS AN INITIAL PRESENTATION OF LUNG CANCER CAUSING MALIGNANT PERICARDIAL EFFUSION

SESSION TITLE: Medical Student/Resident Lung Cancer Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pericardial effusion is a devastating cardiac condition, resulting from various etiology. Cardiac arrhythmia is an uncommon presentation of pericardial effusion, while atrial fibrillation is the most common arrhythmia found in this condition. Atrial flutter, as an initial presentation of malignant pericardial effusion, has not yet been reported. We presented a case of an elderly man with atrial flutter from malignant cardiac effusion from a newly diagnosed lung cancer. CASE PRESENTATION: An 81-year-old man, with chronic obstructive pulmonary disease and hypertension, presented with acute onset shortness of breath. He used albuterol MDI but his symptoms were not improved. On evaluation, he had heart rate 179 beats per minute (bpm), blood pressure 172/118 mmHg without pulsus paradoxus, and respiratory rate of 26. He had good mental status and did not have jugular venous distention. Lungs exam was normal. Heart exam revealed tachycardia without murmur. His blood test was unremarkable. His ECG showed atrial flutter with rapid ventricular rate and 2:1 block. He received intravenous Diltiazem 20 mg and his heart rate decreased to 90. Point of care ultrasound (POCUS) showed large pericardial effusion without tamponade physiology and no signs of pulmonary edema. Computed tomography (CT) chest illustrated large pericardial effusion with new left upper lung mass. Cytology from pericardial effusion revealed squamous cell carcinoma. He was diagnosed as malignant pericardial effusion from advance stage squamous cell lung cancer. His hospital course was complicated with septic shock and eventually death. DISCUSSION: Lung cancer is the most common metastasis cancer to the heart and pericardium because of the proximity of the tumor to the heart [1]. There are several possible explanations of malignant pericardial effusion pathogenesis. First, it can be a result of cardiac lymphatic drainage occlusion by the tumor [2]. Second, local or hematogenous spread of the tumor lead to venous blood flow obstruction and an increase in hydrostatic pressure causing pericardial effusion [3]. Third, neoplastic pericardial involvement stimulates an overproduction of pericardial fluid [3]. Pericardial effusion in cancer patients may arise from complications of treatment, including chemotherapy and radiation, and hypoalbuminemia from malignancy-related cachexia. Cytology analysis of pericardial fluid and pericardial biopsy should be performed to confirm the diagnosis. Management includes pericardiocentesis, pericardial window, pericardial sclerosis, and radiation therapy. CONCLUSIONS: We presented a rare case of atrial flutter secondary to malignant pericardial effusion from newly diagnosis of advanced-stage lung cancer. Clinicians should have pericardial effusion as a differential diagnosis of patients with atrial flutter as this is a catastrophic condition, requiring urgent management. Reference #1: DeCamp MM, et al. Malignant effusive disease of the pleura and pericardium. Chest. 1997;112(4 Suppl):2915-2955. Reference #2: Chiles C, et al. Metastatic involvement of the heart and pericardium: CT and MR imaging. Radiographics. 2011;21(2):438-449. Reference #3: Scheinin SA, Sosa-Herrera J. Cardiac tamponade resembling an acute myocardial infarction as the initial manifestation of metastatic pericardial adenocarcinoma. Methodist Debakey Cardiovasc J. 2014; 10:124–128. DISCLOSURES: No relevant relationships by Nehad Shabarek, source=Web Response No relevant relationships by Kulachanya Suwanwongse, source=Web Response

Pulsus Alternans as a Sign of Right Ventricular Failure After Left Ventricular Assist Device Implantation

Temporary left ventricular assist devices such as the ImpellaTM are increasingly used in patients with cardiogenic shock. The right ventricle remains the Achilles heel of left ventricular assist device-supported circulation. However, right ventricular failure after implantation of a left ventricular assist device remains incompletely defined and understood. We describe the first case of pulsus paradoxus emerging after the initiation of circulatory support using a left ventricular ImpellaTM device, which is an early sign of right ventricular failure, that was completely abolished after the addition of a temporary right ventricular assist device.

Paradoxical pulse

For thousands of years, palpation of the peripheral pulse was the most important source of information for the physicians about their patients' circulation. The rate, amplitude, and pattern of the pulse served as a basis of amazing observations, although several of them have been also confirmed and substantiated by modern medicine. One of the classical signs is "paradoxical pulse" (PP), which signals potentially life-threatening conditions with various mechanisms in certain diseases. In our review, we demonstrate the pathophysiological bases of PP, and show the equivalents of this sign provided by modern medical equipments. Orv Hetil. 2020; 161(38): 1629-1635.

Respiratory Fluctuation of Peak Systolic Velocities in the Carotid Doppler Waveforms of Patients With Obstructive Airway Disease: Evidence of Pulsus Paradoxus With Experimental Validation.

To characterize fluctuations in peak systolic velocities (PSVs) in Doppler waveforms of the carotid artery in patients with and without obstructive airway disease and in volunteers subjected to incremental levels of airway resistance in an experimental model. The PSV variation in common carotid waveforms was measured in 100 patients who had had a carotid ultrasound examination and no respiratory or carotid disease. This was compared to that of patients who had this study during an admission for acute exacerbation of chronic obstructive pulmonary disease (COPD). The PSV variation was correlated with pulmonary function testing. In addition, 14 healthy volunteers were asked to breathe through 5 resistors. Simultaneous recordings were made of Doppler waveforms in the common carotid artery, cardiac activity, and respiration. Peak systolic velocity changes from inspiration to expiration were calculated. Of the 100 patients without respiratory disease, the magnitude of the PSV variation averaged 6.3 cm/s. Of the 33 patients with COPD, the PSV variation averaged 16.5 cm/s. Nineteen of the 33 patients with COPD had concurrent pulmonary function testing; there was a statistically significant correlation between the PSV variation and forced vital capacity and forced expiratory volume indices. For the volunteers, mean velocity changes were 7.1, 6.6, 8.3, 15.1, and 16.1 cm/s for 0.00-, 2.15-, 3.27-, 3.58-, and 5.77-cm H2 O/L/s levels of breathing resistance, respectively. There was a statistically significant relationship between an increasing airway load and the decline in PSV during inspiration (P = .02). The PSV variation is greater in patients with increased airway resistance. Similar changes are evident in volunteers breathing into resistors. These findings likely reflect pulsus paradoxus.