Preoperative and anesthetic management of high-risk cardiovascular complications of mediastinal masses: a narrative review

Introduction

Rationale and background

The mediastinal space is a highly complex anatomical region, comprising important anatomical structures including the heart, aorta, superior vena cava (SVC), trachea and mainstem bronchi. Space-occupying mediastinal lesions include a range of benign and malignant tumors, from thymomas to lymphomas to thyroid masses, which can manifest with a variety of cardiorespiratory complications. Mass effect within the mediastinum may present with life-threatening complications such as cardiac tamponade, mediastinal mass syndrome (MMS), SVC syndrome, and right ventricular outflow tract (RVOT) obstruction, all of which carry significant morbidity and mortality (1-4). Optimal management of these myriad complications is varied and often not well represented in current guidelines. Given the high morbidity and mortality of cardiovascular complications secondary to mediastinal mass effect, the following review hopes to provide increased clarity into the pathophysiology and management considerations.

Objectives

This review aims to present a comprehensive overview of mediastinal masses and further discussion of management of common cardiovascular complications of mediastinal masses. We present this article in accordance with the Narrative Review reporting checklist (available at https://med.amegroups.com/article/view/10.21037/med-2025-1-66/rc).

Methods

A comprehensive literature search was conducted to review all relevant articles in the database PubMed pertaining to cardiovascular complications related to mediastinal masses (Table 1). The search included key terms of mediastinal masses, cardiac tamponade, SVC syndrome, MMS, and RVOT obstruction. Citations from the search were then exported to a Zotero library, and duplications were identified and removed. Relevant articles published from 2007 to November 2025 were then reviewed by the authors and utilized in writing this narrative review. Only articles published in English language and with the full text available were included. Articles published from 2007 to the publication of this article were included in an effort to focus on current literature on this topic.

Incidence

Space-occupying mediastinal lesions are rare entities ranging from cancerous to benign tissue growths. Overall, thymoma, neurogenic tumors, and benign cysts account for about 60% of mediastinal masses. Thymic neoplasms, thyroid masses, and lymphomas are the most common in adults, while neurogenic tumors, germ cell neoplasms, and foregut cysts are the most common in children (5). The mediastinum is commonly divided into anterior, middle, and posterior components (Figure 1). Anterior mediastinal masses are the most common, accounting for about half of all masses, and commonly include thymomas, teratomas, lymphomas, and thyroid masses (5). Congenital cysts are the most prevalent type of middle mediastinal mass, while neurogenic tumors account for the majority of posterior mediastinal masses (5). Lymph node enlargement and metastatic disease are also important considerations with differential diagnosis. Thymomas are the most common lesion type overall (27.8%), followed by benign mediastinal cysts (20%) and lymphomas (16.1%) (6). Lymphoma, including both Hodgkin’s and non-Hodgkin’s lymphoma, is the most common malignant mediastinal tumor, and may account for up to 60% of all malignant mediastinal masses (7). Furthermore, infections, including tuberculosis and histoplasmosis, can contribute to fibrosing mediastinitis, which has also been reported to present as a mediastinal mass and can compress mediastinal structures depending on the extent of fibrosis (8).

Figure 1 Mediastinal mass compartments, with common etiologies of each. The mediastinum is divided into the anterior, middle, and posterior mediastinum, with the majority of mediastinal masses arising from the anterior compartment.

Workup

Clinical presentation of mediastinal masses is highly variable and may mimic other medical conditions. Therefore, utilizing a structured approach in assessing these patients is key to ensuring appropriate and timely management, as outlined in Figure 2. A thorough history and physical exam is important, including the identification of key demographics such as age and gender, as the incidence of mediastinal masses and their respective etiologies vary within these characteristics. Common symptoms, although non-specific, include cough, chest pain, fever, chills, and dyspnea (5). Larger masses accompanied by extrinsic compression of vital intra-thoracic organs or tumor invasion may precipitate more severe presentations, including cardiac tamponade or SVC syndrome. Based on clinical suspicion, adjunctive tests such as thyroid function tests, alpha-fetoprotein, beta-human chorionic gonadotropin, and lactate dehydrogenase should be considered for further workup of likely malignancies (9).

Figure 2 Recommended workup for mediastinal masses. Following a thorough history and physical exam, diagnostic assessment should include CT imaging, with additional imaging or lab workup as appropriate based on the likely etiology (5,7,9). Definitive management is determined following tissue diagnosis and ranges from surgical intervention to radiation therapy. AFP, alpha-fetoprotein; beta-hCG, beta-human chorionic gonadotropin; CT, computed tomography; LDH, lactate dehydrogenase; MRI, magnetic resonance imaging; PET/CT, positron emission tomography/computed tomography; SVC, superior vena cava; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Given the wide variability in the etiologies of mediastinal masses, various imaging modalities are invaluable to establishing a definitive diagnosis. Conventional radiography, such as chest radiography, may incidentally pick up some mediastinal masses, and having a two-view chest radiograph can help distinguish the mediastinal compartment the mass is located in and thus narrow the differential (10). While chest radiography may often reveal a lesion or a widened mediastinum, cross-sectional imaging with computed tomography (CT) or magnetic resonance imaging (MRI) is the gold standard imaging modality (5). Important characteristics include size, contour, heterogeneity, presence of solid, cystic, and/or necrotic components, calcification, and involvement of adjacent structures (5). CT imaging can help identify lymphadenopathy and involvement of local structures including the lungs, vasculature, and bones (10). Diffusion-weighted imaging on MRI can also help determine cellularity and provide additional diagnostic yield in distinguishing between solid and cystic masses, which constitutes a significant advantage over CT (5,10,11). Fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) is another imaging modality that often has limited utility in diagnosing mediastinal masses, as fluorodeoxyglucose uptake is nonspecific and can be seen in many inflammatory or infectious conditions (10). While PET/CT is not commonly used to diagnose mediastinal masses, it may be an important consideration for staging lymphoma (6).

Echocardiography has also been investigated as a diagnostic tool for anterior mediastinal masses, which can provide useful information on the associated cardiovascular impact on mediastinal masses and visualization of structures (12). Compared to CT and MRI, transthoracic echocardiography (TTE) and contrast-enhanced ultrasonography are easier to obtain as non-invasive, radiation-free imaging modalities (12). TTE accurately localizes mediastinal masses, characterizes echogenicity and composition, is superior in identifying cystic lesions when compared to CT, and accurately defines anatomic relationships between mediastinal masses, the heart, and major vascular structures (12,13). However, a prior study has shown that larger mediastinal mass sizes were significantly underestimated on TTE, and masses of the posterior mediastinum were difficult to view (12). Studies comparing transesophageal echocardiography (TEE) versus TTE for the detection of mediastinal masses concluded that TEE provides better detection and characterization of masses, including anatomic relationship and hemodynamically significant compression of adjacent structures (13-15). TTE and TEE are thus both useful supplementary imaging tools to better categorize relationships to the heart and surrounding vasculature; however, CT and MRI remain the gold standard diagnostic modalities.

Cardiac tamponade

Cardiac tamponade is caused by progressive external compression of the cardiac chambers, potentially leading to fatal hemodynamic compromise. The classic presenting signs and symptoms include Beck’s triad: defined as the presence of jugular venous distention (JVD), muffled heart sounds, and hypotension. However, it should be noted that few cases present with the complete triad, with only 53–88% of cases presenting with JVD, 24–34% with muffled heart sounds, and 14–35% with hypotension (16,17). Additional findings include tachycardia and pulsus paradoxus, which describes a decrease in systolic blood pressure of greater than 10 mmHg upon inspiration, and electrocardiogram may show electrical alternans and decreased voltage (18,19). Imaging including bedside point-of-care ultrasound and formal TTE are crucial aids in diagnosis. Common echocardiogram findings of tamponade include early diastolic collapse of the right ventricle, late diastolic collapse of the right atrium, dilated inferior vena cava (IVC) with minimal respiratory variation, greater than 40% increase in blood flow across the tricuspid valve with inspiration, and greater than 25% decrease in blood flow across the mitral valve during inspiration (18). The most common etiology includes accumulation of fluid within the pericardial space, often due to hemorrhage, aortic dissection, malignant effusions, infection, or autoimmune disease (1). External compression due to mass effect represents a rare but important cause of tamponade physiology, and has been described in multiple case reports (2,20-22). While the standard of care for cardiac tamponade caused by pericardial fluid accumulation is often urgent pericardiocentesis, the management of tamponade due to mass effect with concomitant pericardial effusion is more complex. Tamponade in the setting of a mediastinal mass can be due to both extrinsic compression in addition to fluid accumulation secondary to the tumor. In these patients, the pericardial effusion has been hypothesized to provide a buffer between the mediastinal mass and right ventricular wall (1). Prior case reports have reported a paradoxical worsening of symptoms and hemodynamic status following pericardiocentesis in these patients, leading to increased direct mass effect, resulting in worsened right heart compression, hemodynamic instability, and tamponade physiology (1,2,20). As with cardiac tamponade due to pericardial effusions, these patients require sufficient preload to maintain venous return and cardiac output (1). While no guidelines currently exist regarding optimal pericardial fluid removal in these patients, careful consideration of small-volume or serial pericardiocentesis may be preferred to maintain some of the fluid buffer against direct mass effect (1,2). Several case reports have demonstrated improvement in symptoms and tamponade physiology after definitive therapy through surgical resection, radiation, or chemotherapy (21,22). Thus, these patients require a multidisciplinary approach to determine the optimal treatment strategy according to the underlying etiology of the accompanying mediastinal mass.

MMS

MMS represents a life-threatening syndrome seen after the initiation of positive pressure ventilation in patients with mediastinal masses. Several cases of MMS have been seen perioperatively as a result of anesthesia and intubation. While some cases of MMS can be asymptomatic, cases can range in clinical presentation based on the location and characteristics of the mediastinal mass, including cough, dysphagia, and syncope to life-threatening hemodynamic collapse (3,23). Upon intubation and initiation of positive pressure ventilation, patients with MMS can present with worsening hemodynamics due to decreased venous return and cardiac output as well as increased compression of mediastinal structures (1,11). Patients with mediastinal masses, particularly those with pre-existing obstruction due to intrathoracic mass effect, can develop severe cardiopulmonary compromise and obstructive shock (1,24). In severe cases, patients can also progress to cardiopulmonary arrest, and traditional advanced cardiac life support may be ineffective as chest compressions may further compress the heart chambers and preclude adequate ventricular filling (1).

General anesthesia induction in patients with mediastinal masses may also cause decreased tone of the major airways leading to progressive cardiorespiratory compromise and difficulty with ventilation (25). Positional changes during the induction process can also contribute to the pathophysiology. Induction of anesthesia typically places patients in the supine position, which can contribute to the compressive effects of a mediastinal mass due to gravity (11,26,27). The use of sedation and/or muscle relaxants with induction further leads to decreased respiratory and diaphragm muscle tone and should be avoided when possible (11,25). One prior study has also recommended the use of inhalation induction, as this is thought to help maintain spontaneous ventilation compared to intravenous anesthesia induction (25). In cases where spontaneous ventilation is compromised, positive pressure ventilation and positive end-expiratory pressure (PEEP) are important tools to maintain ventilation. Positive pressure ventilation increases peak inspiratory flow and thus keeps central airways open, and additional PEEP can prevent airway collapse during expiration (25). Due to the compressive effect of mediastinal masses, it is crucial to adjust ventilator settings to prolong the expiratory phase to prevent air trapping and subsequent airway collapse (25). To avoid the need for general anesthesia induction, several case reports have demonstrated the efficacy of awake fiberoptic intubation with the use of local anesthesia only, which maintains spontaneous respiration and also allows for direct visualization of the airway (3,11). A rigid bronchoscope may be necessary to confirm bypass of the area of obstruction (11,25,28). Use of an adjustable surgical table, short-acting anesthetic agents with slow administration, avoidance of muscle relaxants and paralytics, and use of spontaneous ventilation modes are also important perioperative considerations to prevent MMS (3,4,25). Patient positioning is also an important consideration, as lateral decubitus or prone positioning may be useful, depending on mediastinal mass location, to reduce mass effect (11).

Early multidisciplinary planning, including critical care, anesthesia, radiology, and cardiothoracic surgery, is paramount in ensuring appropriate resources are available in the management of these patients. In cases where MMS is precipitated by anesthesia induction or intubation, the patient should be emergently stabilized by the interdisciplinary medical team. Adequate venous return is critical, and extracorporeal life support should be considered as early as possible (24). Extracorporeal membrane oxygenation (ECMO) support equipment and clinical engineering and perfusionist staff should be available throughout cases, particularly in higher-risk patients with known compression of the trachea, mainstem bronchi, great vessels, or heart (11,25). Obtaining pre-emptive or early access in case cannulation for ECMO is needed is also an important consideration (11). Large-bore venous access of the lower extremities, often the femoral vein, is preferred due to the risk of SVC syndrome and risk of impaired medication administration and circulation via the upper extremities (11,28). Several reports have shown ECMO to be an effective temporary cardiorespiratory stabilization method in patients with large mediastinal masses and impending hemodynamic collapse (28,29). Additionally, positional changes, including the Fowler’s position, prone positioning, and left lateral decubitus position, have all been hypothesized to improve hemodynamics (11).

SVC syndrome

SVC syndrome is due to partial or complete obstruction of blood flow within the SVC, leading to a variety of clinical symptoms. The SVC is an important anatomical structure that accounts for approximately one-third of cardiac venous return (26). Due to its thin-walled, compliant nature, the SVC is especially susceptible to extrinsic compression. An estimated 15,000 cases occur annually in the US, and malignancy is a leading cause, accounting for 65–70% of cases (26,27). Primary lung malignancies account for 75–80% of cases, although mediastinal masses can occasionally also cause SVC syndrome. Lymphoma, most commonly non-Hodgkin’s lymphoma, accounts for 10–15% of malignancy-related SVC syndrome cases due to mediastinal masses (26,30). Thymoma, germ cell tumors, and solid tumors with mediastinal lymph node metastasis together comprise the remaining ~15% of cases (30). SVC syndrome can present with various neurologic, vascular, and respiratory symptoms. Typical neurologic signs may include headache, dizziness, syncope, and obtundation (27). Vascular symptoms include facial plethora, upper extremity edema, and JVD, while respiratory symptoms include dyspnea, cough, stridor, and hoarse voice (27,31). Provocative maneuvers that increase intrathoracic pressure or venous return, including Valsalva maneuver, supine positioning, and leg elevation, can exacerbate symptoms (27,31). The timing of obstruction often predicts symptom severity, as the body will adapt through formation of venous collaterals to increase venous return. Given that such collaterals often take weeks to develop, rapid obstruction is more likely to present with more acute and severe symptomology (26). While normal central venous pressure in the SVC is typically 2–8 mmHg, SVC obstruction can cause elevated pressures as high as 20–40 mmHg (26,30). While not often fatal, with death estimated to occur in just 3 in 1,000 cases (26), SVC syndrome leading to obstructive shock, laryngeal edema with consequent respiratory failure, and cerebral edema leading to coma represent medical emergencies (27). The development of SVC syndrome also represents an important poor prognostic factor, as median survival after diagnosis in malignancy-related SVC syndrome is just 6 months (30). The severity of SVC syndrome can be graded, with Yu et al. proposing a scoring system as well as the Kishi score, based on symptom severity (30,32), with higher scores indicating more urgent endovascular intervention. There are also anatomic classifications of obstruction based on obstruction positioning relative to the azygos vein (30).

Advanced imaging is the mainstay of diagnosis, including chest radiography, CT, venography, MRI, and duplex ultrasonography. While venography including digital subtraction venography has previously been considered the standard, CT chest with delayed contrast can assist with diagnosis, provide information regarding etiology, and define collateral vessels while also differentiating thrombosis from extrinsic compression (26,27,30,33). Initial treatment should focus on airway stabilization and hemodynamic support (30), followed by a multidisciplinary approach aimed at treating both the obstruction and underlying cause. Respiratory failure in patients with SVC syndrome presents a challenging clinical scenario, as the increased intrathoracic pressure with intubation and mechanical ventilation can hypothetically worsen obstruction. ECMO should be considered for worsening hypoxemia in these cases (34). Patients with mediastinal mass and SVC syndrome who require general anesthesia are at high risk of complications as up to 20% of patients can develop serious complications related to airway and vascular structure compression, with tracheal compression being one of the highest risk factors (31). Similar to MMS, maintaining spontaneous ventilation and avoiding paralytics is recommended, and dexmedetomidine use has been shown in previous reports to provide adequate anesthesia while maintaining spontaneous ventilation (31). In non-life-threatening situations without a tissue-proven diagnosis, tissue sampling should be pursued on an urgent basis to help direct therapy (30,35). First-line management for these non-life-threatening cases often includes targeted chemoradiation to improve symptoms and reduce disease burden (30). Reports have demonstrated symptomatic improvement following chemotherapy initiation in treating SVC syndrome caused by lymphoma (36). In contrast, life-threatening cases often indicate urgent endovascular intervention to address the obstruction (30). Additional therapies such as glucocorticoids and loop diuretics are commonly used to alleviate associated edema; however, the data to support their efficacy are limited (30). Prior to the more widespread use of endovascular intervention, radiation therapy had been considered the first-line treatment to rapidly reduce obstruction-related symptoms, and while it was effective in about 80% of patients, the effects may take days to weeks to manifest (30). Endovascular therapy with balloon angioplasty and/or stenting is now considered the standard of care, given its high success rate with relatively low risk of complications as well as more rapid relief of symptoms (30). Patients with thrombosis in addition to SVC syndrome should be treated with thrombectomy or thrombolysis prior to revascularization. In cases with extensive thrombosis or anatomy not amenable to revascularization, open surgical bypass grafting and SVC reconstruction can be considered (30,37).

RVOT obstruction

A rarer manifestation of mediastinal masses includes extrinsic compression of the major pulmonary arteries, which can lead to pulmonary hypertension and RVOT obstruction (38). Blood flows from the right ventricle into the pulmonary arteries, and compression of pulmonary arteries by mass effect can cause pulmonary artery narrowing, creating an acquired pulmonary stenosis. Over time this can present with pulmonary artery hypertension and associated increase in right ventricular afterload (38). Symptoms of RVOT obstruction depend on the etiology and can include chest pain, fatigue, dyspnea, and syncope (39). Additionally, compression of the pulmonary artery can cause hypoxemia by impairing gas exchange via ventilation and perfusion mismatch (40). In most cases, RVOT obstruction can be reversible once the cause is identified and treated (41). Existing literature supports the use of echocardiography as an important diagnostic tool to identify extrinsic masses with concomitant RVOT obstruction (42). Several case reports examining patients with malignancy-associated RVOT obstruction conclude that appropriate treatment with chemotherapy often leads to full resolution of adverse hemodynamic effects, which is evident on follow-up interval echocardiography (38,43). In cases of hemodynamic compromise where cancer therapy is not appropriate, other reports have recommended utilizing ECMO for hemodynamic support (44). There are also rare cases of pulmonary artery stenting in a case of mediastinal mass contributing to acute respiratory distress syndrome with subsequent improvement in the PaO₂/FiO₂ ratio (40). Furthermore, surgical resection can be an option for masses directly compressing the RVOT, especially in cases where chemotherapy does not provide immediate improvement (45).

Definitive management

Given the numerous etiologies of mediastinal masses, tissue biopsy is often critical to confirm a histopathologic diagnosis and guide further management (Table 2). Certain etiologies, including thyroid goiter, benign teratoma, and thymoma, are commonly diagnosed by classic imaging findings, and biopsy is not routinely indicated (9). Various techniques can be considered based on mass location, including ultrasound or percutaneous image-guided biopsy, mediastinoscopy, and either open or video-assisted thoracoscopic surgical approaches (11). For patients deemed high risk for MMS, biopsy under local anesthesia is often preferred (11). Masses located in the anterior or posterior compartments of the mediastinum can often be biopsied with ultrasound or CT-guided core needle biopsy, while masses of the middle mediastinum often require endobronchial or esophageal endoscopic ultrasound-guided needle aspiration (52). Surgical biopsy, ranging from minimally invasive to open approaches, often provides more adequate tissue sampling and reduces the risk of false negative results (52). It is also the recommended approach for patients with irregular, large tumors and tumors invading local mediastinal structures (52). The tumor size and precise location often dictate whether minimally invasive approaches such as anterior mediastinoscopy or thoracoscopy are favored compared to partial sternotomy or limited thoracotomy, and multidisciplinary planning is crucial (52). Sampling of pleural or pericardial effusions and biopsy of lymph nodes may also provide diagnostic information, and can be useful in patients deemed high risk for MMS with anesthesia induction (11).

All patients with thymoma should undergo surgical resection if feasible, and neoadjuvant chemotherapy and/or radiotherapy have been shown to effectively reduce tumor volume prior to resection (9,11,28). Benign teratomas and thymic lesions can be observed if asymptomatic; however, surgical resection can be considered if symptomatic or in the presence of thymoma-associated myasthenia gravis (9). For other etiologies, histopathologic diagnosis is crucial to guide further management, as neoadjuvant therapy should be utilized to reduce tumor burden and facilitate surgical resection (28). For cases of malignant lymphoma, tissue sampling is needed to determine optimal treatment, and early initiation of appropriate chemotherapy has been shown to significantly improve survival (11,21,27). Malignant germ cell seminomas typically respond to both chemotherapy and radiotherapy, while non-seminomatous germ cell tumors are treated with chemotherapy followed by surgical resection of residual tumor (11,28). In cases of symptomatic neurogenic tumors, cystic lesions or well-encapsulated solid tumors can be managed with complete surgical resection without the need for preceding biopsy (50). While the majority of neurogenic tumors are benign, malignant lesions have been treated with post-resection radiation therapy in several case reports (51). Thyroid masses can range from benign thyroid goiter to various malignant lesions, including thyroid carcinoma (47). Surgery is a mainstay of treatment for thyroid lesions, and systemic therapy, including radioiodine therapy, chemotherapy, and/or radiotherapy, may also be used (47,48). Regardless of etiology, interdisciplinary discussion including oncology, surgery, radiation oncology, and critical care is crucial for optimal management, particularly in the presence of life-threatening hemodynamic complications.

Conclusions

Mediastinal masses, while rare, can range in clinical presentation from asymptomatic to major cardiovascular compromise. Proper workup, including a thorough history and physical exam, is essential as the presentation of mediastinal masses can be highly variable. Several imaging modalities are effective in diagnosing mediastinal masses, primarily CT and MRI, as well as echocardiography, which may provide additional insight into surrounding effusions and impending tamponade physiology. Major cardiovascular complications can include cardiac tamponade, MMS, SVC syndrome, and RVOT obstruction, which can be life-threatening. Management of mass-related complications requires acute stabilization and awareness of the reduced hemodynamic reserve with significant intrathoracic mass effect. Definitive therapy requires identifying the underlying etiology and careful interdisciplinary collaboration.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://med.amegroups.com/article/view/10.21037/med-2025-1-66/rc

Peer Review File: Available at https://med.amegroups.com/article/view/10.21037/med-2025-1-66/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://med.amegroups.com/article/view/10.21037/med-2025-1-66/coif). The authors have no conflicts of interest to declare.

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