Tachycardia as an Early Clinical Sign of Pulmonary Embolism: A Case of Unprovoked Massive Bilateral Pulmonary Embolism “Saddle’’ Embolismin a Young Adult

preprint OA: closed
Full text JSON View at publisher
Full text 32,735 characters · extracted from preprint-html · click to expand
Tachycardia as an Early Clinical Sign of Pulmonary Embolism: A Case of Unprovoked Massive Bilateral Pulmonary Embolism “Saddle’’ Embolismin a Young Adult | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Tachycardia as an Early Clinical Sign of Pulmonary Embolism: A Case of Unprovoked Massive Bilateral Pulmonary Embolism “Saddle’’ Embolismin a Young Adult Ayisha Ameen, Ajal Salam, Dina Sheko This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7346902/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Pulmonary embolism (PE) is a potentially fatal condition presenting with various symptoms. Typical features include sudden-onset dyspnea, pleuritic chest pain, and hemoptysis; however, atypical presentations may delay diagnosis. A massive PE caused by a saddle thrombus at the pulmonary trunk bifurcation—as in our case—may present with syncope, presyncope, hypotension, and can progress to circulatory collapse and shock. We present a 47-year-old female with bronchial asthma who presented with sore throat and shortness of breath. Despite lacking traditional risk factors or symptoms, a borderline unexplained tachycardia (HR 105 bpm) prompted further workup. Elevated D-dimer and CT pulmonary angiography identified a massive bilateral saddle embolus with right heart strain. The patient underwent thrombolysis and recovered fully. This case highlights the critical importance of considering tachycardia as a sole early PE indicator in the emergency setting. Tachycardia Massive Pulmonary Embolism Saddle embolis Figures Figure 1 Figure 2 Background Pulmonary embolism is a critical diagnosis in emergency medicine, typically manifesting with acute symptoms such as dyspnea, pleuritic chest pain, tachypnoea, haemoptysis, and signs of DVT. Massive PE may present with hypotension, syncope, or signs of right heart strain and can lead to cardiogenic shock. A saddle PE, lodged at the bifurcation of the pulmonary trunk, is a common cause of massive embolism. Diagnosis can be challenging in atypical presentations. This report describes a case in which tachycardia was the only initial clinical clue. Case Presentation A 47 year old female, with a past medical history of bronchial asthma, arrived at our ED with complaints of progressive shortness of breath since 3 days and symptoms of upper respiratory tract infection like sore-throat and cough. Denied any other symptoms. The patient had no history of previous DVT or PE, no history of hypercoagulable state ,no history of prolonged immobilization or long travel, no history of oral contraceptive pill intake, no family history of thrombophilia and no history of smoking or alcohol consumption. Upon initial examination, all vitals of the patient were ,the heart rate, which was borderline tachycardic with a rate of 105 beats per minute. The patient was afebrile on examination with a temperature of 36.4 ℃, respiratory rate (RR) of 24 breaths per minute, Blood Pressure (BP) − 104/84 mmHg, oxygen saturation (SpO2)- 96% in room air. chest examination revealed bi-basilar wheeze and crackles on auscultation.no other significant examination findings .As the patient was waiting for her blood investigations and chest XR to be done ,the patient was notably becoming tachypnoeic with a respiratory rate (RR) of 27 breaths per minute and oxygen saturation (SpO2) had to be maintained with oxygen therapy. The patient’s Modified WELL’S Score was calculated to be 1.5 with tachycardia being the only contributory factor to the above pre-test probability criteria. This led the physician to order a blood investigation to assess the D-dimer levels. The result was an elevated D-dimer which prompted the physician to rule out pulmonary embolism. Subsequently, CT Pulmonary Angiogram was for the patient which revealed a massive bilateral pulmonary embolism with right ventricular strain. [Fig. 1 ].The embolus had lodged itself at the bifurcation of the pulmonary trunk, which is commonly termed as a ‘saddle embolus’. Bedside ECHO revealed a positive McConnel’s Sign, positive D sign, dilated right ventricle and left ventricular hypertrophy. The patient had now progressed to a state of respiratory distress wherein she was unable to talk. Her oxygen saturation (SpO2) at the time was 100% on 15L per minute of O2 supplementation, blood pressure (BP) was 118/78 mmHg and her heart rate (HR) was 107 beats per minute. The patient could now be classified as a case of an “ intermediate high risk pulmonary embolism ” Therapeutic anticoagulation with enoxaparin was initiated and an arterial line insertion was done for accurate blood pressure monitoring. MICU team was onboard for close patient monitoring. treatment with Tissue Plasminogen activator ( TPA )was administered to the patient after ruling out all absolute and relative contraindications against fibrinolytic therapy. The plan was to administer 50mg (half dose) of TPA and to resume therapeutic anticoagulation after the TPA administration. The TPA drug administered in this case was Alteplase. After thrombolysis, the patient was shifted back to the medical ward on the next day to resume therapeutic anticoagulation using Enoxaparin. Upon receiving the patient in the medical ward, it was noticed by the physician that the patient was doing well, had no shortness of breath and was relieved of her initial complaints. Upon clinical examination, all vitals and physical examination were within normal limits.In view of no history of risk factors for PE ,investigations were ordered to rule out any underlying malignancy. USG abdomen and mammogram revealed no obvious focal lesions. The patient was discharged after switching her therapeutic anticoagulant drug from Enoxaparin to Rivaroxaban and was also advised to follow up for an outpatient colonoscopy for age appropriate screening. Discussion Pulmonary embolism can be defined as the luminal obstruction of one or more of the pulmonary arteries, typically but not always associated with deep vein thrombosis 2 . The risk factors that contribute to pulmonary embolism can be broadly classified into thrombotic and non-thrombotic risk factors 2 . Any factor that contributes to the Virchow’s triad of hypercoagulability, endothelial damage and/or venous stasis is indeed a thrombotic risk factor. Transient thrombotic risk factors include prolonged immobilization, surgery under general anesthesia, use of oral contraceptives, hormone replacement therapy, pregnancy, intravascular devices and patient factors like obesity, smoking, IV drug abuse 4 , 5 . Chronic thrombotic risk factors include active cancer, nephrotic syndrome, autoimmune disorders like APLA syndrome and inflammatory bowel disease, hereditary thrombophilia conditions ,patient factors like age > 60 years, previous or family history of DVT or PE and an anatomic predisposition to venous stasis which may be caused due to the mass effect of an underlying malignancy or due to underlying genetic disorders 4 – 7 . Causes of non-thrombotic risk factors are namely fat embolism, air embolism, bacterial embolism, pulmonary tumour embolism, pulmonary cement embolism, amniotic fluid embolism to name a few. Pulmonary embolism typically presents acutely with symptoms such as dyspnea (in over 75% of cases), tachycardia, tachypnea, sudden pleuritic chest pain, hemoptysis, and signs of deep vein thrombosis (e.g., unilateral painful lower limb swelling)1,2. Alternatively, a massive pulmonary embolism—potentially caused by a saddle thrombus at the pulmonary trunk bifurcation as in our case—may present with syncope, presyncope, hypotension, elevated jugular venous pressure, and Kussmaul sign, potentially progressing to circulatory collapse and shock2. Our patient, however, presented atypically with only borderline tachycardia and upper respiratory symptoms. While her asthma explained wheezing and dyspnea, persistent tachycardia prompted calculation of Wells and PERC scores, which led to diagnostic imaging. This case underscores the importance of adherence to clinical decision tools and vigilance when presentations do not match classic patterns. Conclusion Emergency clinicians should maintain a high index of suspicion for pulmonary embolism, including awareness of atypical presentations that may delay diagnosis. Strict adherence to clinical protocols, combined with careful assessment of any deviations in vital signs or examination findings, is essential. As illustrated by our case, isolated tachycardia may be the sole initial sign of a life-threatening PE, underscoring the need for vigilance and timely evaluation. Declarations Ethics approval and consent to participate The article describes a case report. Therefore, no additional permission from our Ethics Committee was required. Consent for publication A verbal consent for publication was obtained. Availability of data and material All data generated or analysed during this study are included in this published article. Competing interests The authors declare that they have no competing interests. Funding This study was not funded. Authors' contributions AA,: Data Collection, Literature Search, Manuscript Preparation AA , Histopathology slides, Manuscript Preparation All authors read and approved the final manuscript. Acknowledgments We thank the patient for allowing us to share his case. References 1. Hirmerova J, Seidlerova J, Chudacek Z. The Prevalence of Concomitant Deep Vein Thrombosis, Symptomatic or Asymptomatic, Proximal or Distal, in Patients With Symptomatic Pulmonary Embolism. Clin Appl Thromb Off J Int Acad Clin Appl Thromb. 2018;24(8):1352-1357. doi:10.1177/1076029618779143 2. Walls RM, Hockberger RS, Gausche-Hill M, Rosen P, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Elsevier; 2023. 3. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011;123(16):1788-1830. doi:10.1161/CIR.0b013e318214914f 4. Piazza G, Goldhaber SZ. Acute pulmonary embolism: part I: epidemiology and diagnosis. Circulation. 2006;114(2):e28-32. doi:10.1161/CIRCULATIONAHA.106.620872 5. Ortel TL, Neumann I, Ageno W, et al. American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism. Blood Adv. 2020;4(19):4693-4738. doi:10.1182/bloodadvances.2020001830 6. Prandoni P, Lensing AW, Cogo A, et al. The long-term clinical course of acute deep venous thrombosis. Ann Intern Med. 1996;125(1):1-7. doi:10.7326/0003-4819-125-1-199607010-00001 7. Al-Azzawi HF, Obi OC, Safi J, Song M. Nephrotic syndrome-induced thromboembolism in adults. Int J Crit Illn Inj Sci. 2016;6(2):85-88. doi:10.4103/2229-5151.183019 8. Han Y, Gong Y. Pulmonary embolism with abdominal pain as the chief complaint. Medicine (Baltimore). 2019;98(44):e17791. doi:10.1097/MD.0000000000017791 https://pmc.ncbi.nlm.nih.gov/articles/PMC3856545/#:~:text=However%2C%20depending%20on%20the%20clinical,aggressive%20therapy%20such%20as%20thrombolysis . Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7346902","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":504993331,"identity":"82d89833-af1a-4465-8a30-e640e0cf3ee8","order_by":0,"name":"Ayisha Ameen","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA50lEQVRIiWNgGAWjYFACxgZmCIP5AJCQkCFFC1sCSAsPUfZAtfAYgEmCyvlnJDd/LqjZJscv3fP51Y0aCx4G9sNHN+DTInEjsU16xrHbxpJzzm6zzjkGdBhPWtoNvNYAtTDzsN1O3HAjd5txDhtQiwSPGV4t8jcSmz/z/Ltdv/9GzjPjnH9EaDG4kdggzdt2O8FAIof5cW4bEVoMzzxsk+btu20440aaGXNunwQPGyG/yB1Pf/yZ59tteWDQPf6c861Ojp/98DH83hdIgDPZJMAkXuUgwH8AzmT+QFD1KBgFo2AUjEgAAHRiSaJzfi8EAAAAAElFTkSuQmCC","orcid":"","institution":"Hamad Medical Corporation","correspondingAuthor":true,"prefix":"","firstName":"Ayisha","middleName":"","lastName":"Ameen","suffix":""},{"id":504993332,"identity":"68383fbc-f1b0-49a4-9e60-7e07f7e8d59a","order_by":1,"name":"Ajal Salam","email":"","orcid":"","institution":"Government Medical College","correspondingAuthor":false,"prefix":"","firstName":"Ajal","middleName":"","lastName":"Salam","suffix":""},{"id":504993333,"identity":"817397bd-ee70-45e8-a149-726b84cf88ae","order_by":2,"name":"Dina Sheko","email":"","orcid":"","institution":"Hamad Medical Corporation","correspondingAuthor":false,"prefix":"","firstName":"Dina","middleName":"","lastName":"Sheko","suffix":""}],"badges":[],"createdAt":"2025-08-11 13:38:14","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-7346902/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-7346902/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":90304118,"identity":"46076cf1-f0da-40d2-b6e0-2b3dea934375","added_by":"auto","created_at":"2025-09-01 09:11:02","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":327654,"visible":true,"origin":"","legend":"\u003cp\u003eMassive bilateral pulmonary embolism , commonly termed as a ‘saddle embolus’.\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-7346902/v1/b711f2c7f1b93167e78631eb.png"},{"id":90304112,"identity":"be49c682-5251-49bc-8c49-62b08ac399b5","added_by":"auto","created_at":"2025-09-01 09:11:02","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":324155,"visible":true,"origin":"","legend":"\u003cp\u003eMultiple filling defects are seen in the main pulmonary trunk, right and left main pulmonary arteries and their segmental branches consistent with massive bilateral pulmonary embolism.\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-7346902/v1/7b203524a637e90a80f9405c.png"},{"id":92418080,"identity":"f9ac672f-3ad4-4881-9a83-f63a411bd6ce","added_by":"auto","created_at":"2025-09-29 13:47:07","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":952765,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7346902/v1/81dc2ff6-598f-4d46-8ddb-02973fc244b5.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Tachycardia as an Early Clinical Sign of Pulmonary Embolism: A Case of Unprovoked Massive Bilateral Pulmonary Embolism “Saddle’’ Embolismin a Young Adult","fulltext":[{"header":"Background","content":"\u003cp\u003ePulmonary embolism is a critical diagnosis in emergency medicine, typically manifesting with acute symptoms such as dyspnea, pleuritic chest pain, tachypnoea, haemoptysis, and signs of DVT. Massive PE may present with hypotension, syncope, or signs of right heart strain and can lead to cardiogenic shock. A saddle PE, lodged at the bifurcation of the pulmonary trunk, is a common cause of massive embolism. Diagnosis can be challenging in atypical presentations. This report describes a case in which tachycardia was the only initial clinical clue.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 47 year old female, with a past medical history of bronchial asthma, arrived at our ED with complaints of progressive shortness of breath since 3 days and symptoms of upper respiratory tract infection like sore-throat and cough. Denied any other symptoms. The patient had no history of previous DVT or PE, no history of hypercoagulable state ,no history of prolonged immobilization or long travel, no history of oral contraceptive pill intake, no family history of thrombophilia and no history of smoking or alcohol consumption.\u003c/p\u003e\u003cp\u003eUpon initial examination, all vitals of the patient were ,the heart rate, which was borderline tachycardic with a rate of 105 beats per minute. The patient was afebrile on examination with a temperature of 36.4 ℃, respiratory rate (RR) of 24 breaths per minute, Blood Pressure (BP) \u0026minus;\u0026thinsp;104/84 mmHg, oxygen saturation (SpO2)- 96% in room air. chest examination revealed bi-basilar wheeze and crackles on auscultation.no other significant examination findings .As the patient was waiting for her blood investigations and chest XR to be done ,the patient was notably becoming tachypnoeic with a respiratory rate (RR) of 27 breaths per minute and oxygen saturation (SpO2) had to be maintained with oxygen therapy. The patient\u0026rsquo;s Modified WELL\u0026rsquo;S Score was calculated to be 1.5 with tachycardia being the only contributory factor to the above pre-test probability criteria. This led the physician to order a blood investigation to assess the D-dimer levels. The result was an elevated D-dimer which prompted the physician to rule out pulmonary embolism. Subsequently, CT Pulmonary Angiogram was for the patient which revealed a massive bilateral pulmonary embolism with right ventricular strain. [Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e].The embolus had lodged itself at the bifurcation of the pulmonary trunk, which is commonly termed as a \u0026lsquo;saddle embolus\u0026rsquo;. Bedside ECHO revealed a positive McConnel\u0026rsquo;s Sign, positive D sign, dilated right ventricle and left ventricular hypertrophy. The patient had now progressed to a state of respiratory distress wherein she was unable to talk. Her oxygen saturation (SpO2) at the time was 100% on 15L per minute of O2 supplementation, blood pressure (BP) was 118/78 mmHg and her heart rate (HR) was 107 beats per minute. The patient could now be classified as a case of an \u0026ldquo;\u003cb\u003eintermediate high risk pulmonary embolism\u003c/b\u003e\u0026rdquo;\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eTherapeutic anticoagulation with enoxaparin was initiated and an arterial line insertion was done for accurate blood pressure monitoring. MICU team was onboard for close patient monitoring. treatment with Tissue Plasminogen activator ( TPA )was administered to the patient after ruling out all absolute and relative contraindications against fibrinolytic therapy. The plan was to administer 50mg (half dose) of TPA and to resume therapeutic anticoagulation after the TPA administration. The TPA drug administered in this case was Alteplase. After thrombolysis, the patient was shifted back to the medical ward on the next day to resume therapeutic anticoagulation using Enoxaparin. Upon receiving the patient in the medical ward, it was noticed by the physician that the patient was doing well, had no shortness of breath and was relieved of her initial complaints. Upon clinical examination, all vitals and physical examination were within normal limits.In view of no history of risk factors for PE ,investigations were ordered to rule out any underlying malignancy. USG abdomen and mammogram revealed no obvious focal lesions.\u003c/p\u003e\u003cp\u003eThe patient was discharged after switching her therapeutic anticoagulant drug from Enoxaparin to Rivaroxaban and was also advised to follow up for an outpatient colonoscopy for age appropriate screening.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003ePulmonary embolism can be defined as the luminal obstruction of one or more of the pulmonary arteries, typically but not always associated with deep vein thrombosis\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e. The risk factors that contribute to pulmonary embolism can be broadly classified into thrombotic and non-thrombotic risk factors\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e. Any factor that contributes to the Virchow\u0026rsquo;s triad of hypercoagulability, endothelial damage and/or venous stasis is indeed a thrombotic risk factor. Transient thrombotic risk factors include prolonged immobilization, surgery under general anesthesia, use of oral contraceptives, hormone replacement therapy, pregnancy, intravascular devices and patient factors like obesity, smoking, IV drug abuse\u003csup\u003e\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e,\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e. Chronic thrombotic risk factors include active cancer, nephrotic syndrome, autoimmune disorders like APLA syndrome and inflammatory bowel disease, hereditary thrombophilia conditions ,patient factors like age\u0026thinsp;\u0026gt;\u0026thinsp;60 years, previous or family history of DVT or PE and an anatomic predisposition to venous stasis which may be caused due to the mass effect of an underlying malignancy or due to underlying genetic disorders\u003csup\u003e\u003cspan additionalcitationids=\"CR5 CR6\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e. Causes of non-thrombotic risk factors are namely fat embolism, air embolism, bacterial embolism, pulmonary tumour embolism, pulmonary cement embolism, amniotic fluid embolism to name a few.\u003c/p\u003e\u003cp\u003ePulmonary embolism typically presents acutely with symptoms such as dyspnea (in over 75% of cases), tachycardia, tachypnea, sudden pleuritic chest pain, hemoptysis, and signs of deep vein thrombosis (e.g., unilateral painful lower limb swelling)1,2. Alternatively, a massive pulmonary embolism\u0026mdash;potentially caused by a saddle thrombus at the pulmonary trunk bifurcation as in our case\u0026mdash;may present with syncope, presyncope, hypotension, elevated jugular venous pressure, and Kussmaul sign, potentially progressing to circulatory collapse and shock2. Our patient, however, presented atypically with only borderline tachycardia and upper respiratory symptoms. While her asthma explained wheezing and dyspnea, persistent tachycardia prompted calculation of Wells and PERC scores, which led to diagnostic imaging. This case underscores the importance of adherence to clinical decision tools and vigilance when presentations do not match classic patterns.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eEmergency clinicians should maintain a high index of suspicion for pulmonary embolism, including awareness of atypical presentations that may delay diagnosis. Strict adherence to clinical protocols, combined with careful assessment of any deviations in vital signs or examination findings, is essential. As illustrated by our case, isolated tachycardia may be the sole initial sign of a life-threatening PE, underscoring the need for vigilance and timely evaluation.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe article describes a case report. Therefore, no additional permission from our Ethics Committee was required.\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA verbal consent for publication was obtained.\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and material\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll data generated or analysed during this study are included in this published article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was not funded.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026apos; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAA,: Data Collection, Literature Search, Manuscript Preparation\u003c/p\u003e\n\u003cp\u003eAA , Histopathology slides, Manuscript Preparation\u003c/p\u003e\n\u003cp\u003eAll authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgments\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe thank the patient for allowing us to share his case.\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003e\u003cem\u003e1. Hirmerova J, Seidlerova J, Chudacek Z. The Prevalence of Concomitant Deep Vein Thrombosis, Symptomatic or Asymptomatic, Proximal or Distal, in Patients With Symptomatic Pulmonary Embolism. Clin Appl Thromb Off J Int Acad Clin Appl Thromb. 2018;24(8):1352-1357. doi:10.1177/1076029618779143\u003c/em\u003e\u003c/li\u003e\n\u003cli\u003e\u003cem\u003e2. Walls RM, Hockberger RS, Gausche-Hill M, Rosen P, eds. Rosen\u0026rsquo;s Emergency Medicine: Concepts and Clinical Practice. Elsevier; 2023.\u003c/em\u003e\u003c/li\u003e\n\u003cli\u003e\u003cem\u003e3. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011;123(16):1788-1830. doi:10.1161/CIR.0b013e318214914f\u003c/em\u003e\u003c/li\u003e\n\u003cli\u003e\u003cem\u003e4. Piazza G, Goldhaber SZ. Acute pulmonary embolism: part I: epidemiology and diagnosis. Circulation. 2006;114(2):e28-32. doi:10.1161/CIRCULATIONAHA.106.620872\u003c/em\u003e\u003c/li\u003e\n\u003cli\u003e\u003cem\u003e5. Ortel TL, Neumann I, Ageno W, et al. American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism. Blood Adv. 2020;4(19):4693-4738. doi:10.1182/bloodadvances.2020001830\u003c/em\u003e\u003c/li\u003e\n\u003cli\u003e\u003cem\u003e6. Prandoni P, Lensing AW, Cogo A, et al. The long-term clinical course of acute deep venous thrombosis. Ann Intern Med. 1996;125(1):1-7. doi:10.7326/0003-4819-125-1-199607010-00001\u003c/em\u003e\u003c/li\u003e\n\u003cli\u003e\u003cem\u003e7. Al-Azzawi HF, Obi OC, Safi J, Song M. Nephrotic syndrome-induced thromboembolism in adults. Int J Crit Illn Inj Sci. 2016;6(2):85-88. doi:10.4103/2229-5151.183019\u003c/em\u003e\u003c/li\u003e\n\u003cli\u003e\u003cem\u003e8. Han Y, Gong Y. Pulmonary embolism with abdominal pain as the chief complaint. Medicine (Baltimore). 2019;98(44):e17791. doi:10.1097/MD.0000000000017791 \u003c/em\u003e\u003cem\u003ehttps://pmc.ncbi.nlm.nih.gov/articles/PMC3856545/#:~:text=However%2C%20depending%20on%20the%20clinical,aggressive%20therapy%20such%20as%20thrombolysis\u003c/em\u003e\u003cem\u003e.\u003c/em\u003e\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Tachycardia, Massive Pulmonary Embolism, Saddle embolis","lastPublishedDoi":"10.21203/rs.3.rs-7346902/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7346902/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003ePulmonary embolism (PE) is a potentially fatal condition presenting with various symptoms. Typical features include sudden-onset dyspnea, pleuritic chest pain, and hemoptysis; however, atypical presentations may delay diagnosis. A massive PE caused by a saddle thrombus at the pulmonary trunk bifurcation\u0026mdash;as in our case\u0026mdash;may present with syncope, presyncope, hypotension, and can progress to circulatory collapse and shock. We present a 47-year-old female with bronchial asthma who presented with sore throat and shortness of breath. Despite lacking traditional risk factors or symptoms, a borderline unexplained tachycardia (HR 105 bpm) prompted further workup. Elevated D-dimer and CT pulmonary angiography identified a massive bilateral saddle embolus with right heart strain. The patient underwent thrombolysis and recovered fully. This case highlights the critical importance of considering tachycardia as a sole early PE indicator in the emergency setting.\u003c/p\u003e","manuscriptTitle":"Tachycardia as an Early Clinical Sign of Pulmonary Embolism: A Case of Unprovoked Massive Bilateral Pulmonary Embolism “Saddle’’ Embolismin a Young Adult","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-09-01 09:10:57","doi":"10.21203/rs.3.rs-7346902/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"ac93f5dc-fadd-49fb-8b65-efab9714c188","owner":[],"postedDate":"September 1st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-09-29T13:38:58+00:00","versionOfRecord":[],"versionCreatedAt":"2025-09-01 09:10:57","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7346902","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7346902","identity":"rs-7346902","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: preprint-html

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2025) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00