COVID-19 and the Risk of Pulmonary Embolism: ECG Findings Can Help

A. Shojaei, A. Karimi
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This fact supports the idea that COVID-19 can cause PE by in-situ immune thrombosis, and the clots might originate from lung vessels rather than deep veins [6]. There is an overlap between signs and symptoms of COVID-19 infection and pulmonary embolism, making the diagnosis of pulmonary embolism challenging [7]. Elevated D-dimer levels may come to our help and increase our suspect for PE, but it is still not specific to the diagnosis of Venous Thromboembolism (VTE) [8]. Anticoagulant therapy may increase the patients’ survival rate [9]. Dyspnea, chest pain, and tachypnea are common in both PTE and COVID-19 infection. Hemoptysis has also been described as a rare COVID clinical symptom (0-5 %) [10], while this number is 13% for patients with PE [11]. In the case reported by Casey et al. [7], a 42 years old COVID-19 positive male presented with pleuritic chest pain, dyspnea, and hemoptysis. In the physical exam, he was tachypneic, and auscultation revealed bibasilar rhonchi. Electrocardiography demonstrated right axis deviation and an S1Q3T3 pattern with flattening of the T-waves in the II, III, aVL and aVF. These findings increased the probability of PE. Also, Laboratory evaluation showed a D-dimer of 4.8μg/dl. So a Computerized Tomography Angiography (CTA) of the chest was obtained. CTA demonstrated bilateral segmental pulmonary emboli and peripheral ground-glass opacities caused by COVID-19 pneumonia. However, sometimes everything becomes more complicated. In the case reported by Ioan et al. [12], a 61 years old male with a history of hypertension treated with Angiotensin-Converting Enzyme Inhibitor (ACEI) presented with dyspnea and cough. His blood pressure was normal, his heart and respiratory rates were 136 and 30, and oxygen saturation was <85% on room air. His Electrocardiogram (ECG) showed sinus tachycardia, ST depression in I, aVL, and V2-V4, and ST-segment elevation in II, III, aVF. An Echocardiography was obtained, which showed RV dilatation, interventricular septal shift, RV lateral wall akinesia, and a pulmonary arterial systolic pressure of >60mmHg. His hypoxemia was refractory to invasive mechanical ventilation, so he was intubated and underwent invasive mechanical ventilation without response. For this patient thrombolytic treatment was started due to suspicion of PE. The patient started improving. CTA confirmed PE with a finding of diffuse bilateral ground-glass opacities consistent with COVID-19 pneumonia. A coronary angiogram showed no significant coronary stenosis. In this case, no obvious sign or symptom, such as pleuritic chest pain or hemoptysis, could lead to PE diagnosis at first. In ECG, there was no flattening of the T-waves or S1Q3T3 pattern, and the patient had a normal axis. Although PE can present with an ST-segment elevation in anteroseptal leads (V1-V4) [13], it is a rare finding that can be mistaken for ST-elevation myocardial infarction. However, in the discussed patient, RV overload and severe pulmonary hypertension with refractory hypoxemia could lead us to PE diagnosis [12]. Conclusion In conclusion, diagnosing COVID-19 complications such as PE can be challenging as COVID-19 can mask their sign and symptoms. We should be aware of any signs or symptoms that can lead us to diagnose these complications. ECG is a low-cost and widely available tool that may give valuable clues to help us diagnose PE. Some ECG signs raise suspicions for PE, such as right axis deviation, S1Q3T3 pattern, or the flattening of T waves. As we saw in an above-discussed case, even an ST-segment elevation in anteroseptal leads can lead us to PE diagnosis.","PeriodicalId":90445,"journal":{"name":"Austin journal of clinical cardiology","volume":"59 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Austin journal of clinical cardiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26420/AUSTINJCLINCARDIOLOG.2021.1073","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

We appreciate the kind invitation to provide an update on an aspect of our study published before [1]. Therefore, we decided to further discuss the Pulmonary Embolism (PE) in patients with COVID-19. COVID-19 pandemic has affected many countries and their health-care system. COVID-19 also imposes significant diagnostic challenges because of its wide range of complications [2]. Evidence shows that COVID-19 can cause a hypercoagulable state and increases the risk of thromboembolism [3]. The radiological appearance of PE in patients with COVID-19 might differ from COVID-19 (-) patients, and the clots are dominantly seen in peripheral zones [4,5]. This fact supports the idea that COVID-19 can cause PE by in-situ immune thrombosis, and the clots might originate from lung vessels rather than deep veins [6]. There is an overlap between signs and symptoms of COVID-19 infection and pulmonary embolism, making the diagnosis of pulmonary embolism challenging [7]. Elevated D-dimer levels may come to our help and increase our suspect for PE, but it is still not specific to the diagnosis of Venous Thromboembolism (VTE) [8]. Anticoagulant therapy may increase the patients’ survival rate [9]. Dyspnea, chest pain, and tachypnea are common in both PTE and COVID-19 infection. Hemoptysis has also been described as a rare COVID clinical symptom (0-5 %) [10], while this number is 13% for patients with PE [11]. In the case reported by Casey et al. [7], a 42 years old COVID-19 positive male presented with pleuritic chest pain, dyspnea, and hemoptysis. In the physical exam, he was tachypneic, and auscultation revealed bibasilar rhonchi. Electrocardiography demonstrated right axis deviation and an S1Q3T3 pattern with flattening of the T-waves in the II, III, aVL and aVF. These findings increased the probability of PE. Also, Laboratory evaluation showed a D-dimer of 4.8μg/dl. So a Computerized Tomography Angiography (CTA) of the chest was obtained. CTA demonstrated bilateral segmental pulmonary emboli and peripheral ground-glass opacities caused by COVID-19 pneumonia. However, sometimes everything becomes more complicated. In the case reported by Ioan et al. [12], a 61 years old male with a history of hypertension treated with Angiotensin-Converting Enzyme Inhibitor (ACEI) presented with dyspnea and cough. His blood pressure was normal, his heart and respiratory rates were 136 and 30, and oxygen saturation was <85% on room air. His Electrocardiogram (ECG) showed sinus tachycardia, ST depression in I, aVL, and V2-V4, and ST-segment elevation in II, III, aVF. An Echocardiography was obtained, which showed RV dilatation, interventricular septal shift, RV lateral wall akinesia, and a pulmonary arterial systolic pressure of >60mmHg. His hypoxemia was refractory to invasive mechanical ventilation, so he was intubated and underwent invasive mechanical ventilation without response. For this patient thrombolytic treatment was started due to suspicion of PE. The patient started improving. CTA confirmed PE with a finding of diffuse bilateral ground-glass opacities consistent with COVID-19 pneumonia. A coronary angiogram showed no significant coronary stenosis. In this case, no obvious sign or symptom, such as pleuritic chest pain or hemoptysis, could lead to PE diagnosis at first. In ECG, there was no flattening of the T-waves or S1Q3T3 pattern, and the patient had a normal axis. Although PE can present with an ST-segment elevation in anteroseptal leads (V1-V4) [13], it is a rare finding that can be mistaken for ST-elevation myocardial infarction. However, in the discussed patient, RV overload and severe pulmonary hypertension with refractory hypoxemia could lead us to PE diagnosis [12]. Conclusion In conclusion, diagnosing COVID-19 complications such as PE can be challenging as COVID-19 can mask their sign and symptoms. We should be aware of any signs or symptoms that can lead us to diagnose these complications. ECG is a low-cost and widely available tool that may give valuable clues to help us diagnose PE. Some ECG signs raise suspicions for PE, such as right axis deviation, S1Q3T3 pattern, or the flattening of T waves. As we saw in an above-discussed case, even an ST-segment elevation in anteroseptal leads can lead us to PE diagnosis.
COVID-19和肺栓塞的风险:心电图检查可以提供帮助
我们感谢您的邀请,为我们在[1]之前发表的研究的一个方面提供更新。因此,我们决定进一步探讨COVID-19患者的肺栓塞(PE)。COVID-19大流行影响了许多国家及其卫生保健系统。COVID-19由于其广泛的并发症,也给诊断带来了重大挑战[2]。有证据表明,COVID-19可导致高凝状态,增加血栓栓塞的风险[3]。COVID-19患者PE的影像学表现可能与COVID-19(-)患者不同,血栓主要见于外周区[4,5]。这一事实支持了COVID-19可通过原位免疫血栓形成导致PE的观点,并且血栓可能起源于肺血管而不是深静脉[6]。COVID-19感染与肺栓塞的体征和症状存在重叠,这使得肺栓塞的诊断具有挑战性[7]。升高的d -二聚体水平可能会对我们有所帮助,并增加我们对PE的怀疑,但它仍然不是静脉血栓栓塞(VTE)诊断的特异性[8]。抗凝治疗可提高患者的生存率[9]。呼吸困难、胸痛和呼吸急促在PTE和COVID-19感染中都很常见。咯血也被描述为罕见的COVID临床症状(0- 5%)[10],而PE患者的这一比例为13%[11]。在Casey等人[7]报道的病例中,一名42岁的COVID-19阳性男性出现胸膜炎性胸痛、呼吸困难和咯血。体检时,他呼吸急促,听诊显示双基底窦性鼻炎。心电图显示右轴偏曲和S1Q3T3型,II、III、aVL和aVF的t波变平。这些发现增加了PE的可能性。此外,实验室评估显示d -二聚体为4.8μg/dl。因此,我们进行了胸部计算机断层血管造影(CTA)。CTA显示由COVID-19肺炎引起的双侧节段性肺栓塞和周围磨玻璃影。然而,有时一切都会变得更加复杂。在Ioan等[12]报道的病例中,一名61岁男性,有高血压病史,接受血管紧张素转换酶抑制剂(Angiotensin-Converting Enzyme Inhibitor, ACEI)治疗,出现呼吸困难和咳嗽。他的血压正常,心跳和呼吸频率分别为136和30,血氧饱和度为60mmHg。患者低氧血症对有创机械通气难治,插管行有创机械通气无反应。该患者因怀疑PE而开始溶栓治疗。病人开始好转。CTA证实PE表现为弥漫性双侧磨玻璃影,与COVID-19肺炎相符。冠状动脉造影未见明显冠状动脉狭窄。在这种情况下,没有明显的体征或症状,如胸膜炎性胸痛或咯血,最初可能导致PE诊断。心电图未见t波平坦或S1Q3T3型,患者轴向正常。虽然PE可在室间隔导联(V1-V4)表现为st段抬高[13],但很少被误认为st段抬高型心肌梗死。然而,在讨论的患者中,RV过载和严重肺动脉高压合并难治性低氧血症可能导致PE诊断[12]。总之,诊断COVID-19并发症(如PE)可能具有挑战性,因为COVID-19可以掩盖其体征和症状。我们应该意识到任何可能导致我们诊断这些并发症的迹象或症状。心电图是一种低成本和广泛使用的工具,可以提供有价值的线索,帮助我们诊断肺动脉栓塞。部分心电图征象,如右轴偏离、S1Q3T3型或T波变平,提示PE的嫌疑。正如我们在上述病例中所看到的,即使是室间隔导联的st段抬高也可以导致PE诊断。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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