A Review of Cardiac Tamponade

Issue 36 | Volume 1

Introduction

The pericardium is comprised of a double-layered serosal membrane, with a visceral layer that covers the surface of the heart and a parietal layer that lays exterior. Pericardial effusions occur when the volume of fluid between these layers exceeds a physiological amount. When this occurs, the pericardial space compresses the heart chambers, which can lead to a medical emergency. If left untreated, cardiac tamponade can cause hemodynamic compromise, cardiac arrest, circulatory shock or death [1].

Etiology and Pathophysiology

There are many causes of pericardial effusions. While effusions are very common after cardiac surgeries, they are rarely large enough to result in tamponade physiology [1, 4]. Sagrista-Sauleda et al reported the most common diagnoses of 322 Spanish patients with moderate to large effusions were: acute idiopathic pericarditis, iatrogenic effusion, malignancy, chronic idiopathic effusion, acute myocardial infarction, end-stage renal disease, congestive heart failure, collagen vascular disease and tuberculosis or bacterial disease [4].

Cardiac tamponade results in hemodynamic compromise due to excessive accumulation of fluid or air in the pericardial sac [6]. The heart is confined by a low compliant pericardial sac. Thus, even a small amount of fluid can increase pericardial pressure [6]. This elevated pericardial pressure applies pressure to the chambers of the heart, leading to diminished diastolic filling and reduced stroke volume. Typically, the right atrium and ventricle are affected earlier on in the development of tamponade due to their thinner, less compliant walls compared to the left side of the heart [2].

Clinical Presentation

When examining a patient, there are certain clinical markers that help indicate cardiac tamponade physiology. In 1935, a thoracic surgeon named Claude Schaeffer Beck described three classical findings for cardiac tamponade – decreased arterial blood pressure, increased jugular venous pressure and distant heart sounds. This became known as the Beck Triad [1-2, 4]. Presenting symptoms can vary depending on how rapidly tamponade physiology occurs, dividing patients into 2 subgroups: acute and subacute.

Acute cardiac tamponade presents with rapid onset of symptoms due to sudden accumulation of pericardial fluid, leading to hemodynamic compromise [1,4]. Clinical symptoms include severe hypotension, tachycardia, and signs of shock. The classic symptoms in Beck’s triad are not always present.

Subacute cardiac tamponade can develop over days or weeks. This allows the pericardium to stretch and become more compliant. A gradual progression may lead to less obvious symptom manifestation. Patients may present with dyspnea, malaise, and peripheral edema. Additionally, pulsus paradoxus, a decrease in systolic blood pressure of more than 10 mmHg during inspiration may be present and is highly specific for tamponade physiology. Jugular venous distention may still be observed, but with varying presentation [1,3,4]. Identifying pertinent signs and symptoms is paramount to the accurate diagnosis and appropriate intervention.

Diagnostic Approach

Point of care ultrasonography (POCUS) is a useful tool to diagnose cardiac tamponade and guide pericardiocentesis in emergent situations. Kearns and Walley described the importance of echocardiographic examination in determining the size, location, and characteristics of pericardial effusions [2]. Additionally, identifying the hemodynamic signs such as late right atrial diastolic collapse (early finding) and early right ventricular diastolic collapse (highly specific). Other echocardiography findings may include a plethoric inferior vena cava indicating elevated central venous pressure, and respiratory variation in mitral and tricuspid valve inflow velocities [2].

In addition to POCUS, electrocardiograms (EKG) and chest radiographs are also useful diagnostic tools. EKG findings for pericardial effusions would include dampened QRS voltage, electrical alternans, arrhythmias, ST-segment elevation, and PR-segment depression. Electrical alternans, while specific, is not highly sensitive. Chest radiographs may appear normal or demonstrate an enlarged cardiac silhouette if the effusion is large [4].

The hemodynamic criteria for diagnosing cardiac tamponade physiology are the equalization of diastolic pressure across all cardiac chambers and evidence for low cardiac output. Pulmonary artery catheters (PAC) can be used to identify hemodynamic profile parameters. For example, PACs can reveal diastolic pressure equalization in the right atrium, right ventricle, pulmonary artery, and pulmonary capillary wedge pressure. Equalization occurs due to increased resistance to the heart from the external compression in the pericardial sac [4].

Management and Stabilization 

Initial stabilization of patients with pericardial effusions causing tamponade is maintaining hemodynamic stability. Fluid resuscitation is essential to increasing preload and optimizing cardiac output. Vasoactive agents may be used in conjunction with intravenous fluids to support blood pressure by increasing peripheral resistance [3]. Bedside echocardiography is an important monitor throughout management and can be useful in guiding fluid resuscitation. [2,6]

The definitive treatment for cardiac tamponade is ultrasound-guided pericardiocentesis to optimize safety and efficacy. This procedure involves percutaneous pericardial fluid drainage to relieve the pressure on the heart [1-2, 5]. In cases such as aortic dissection, trauma, or purulent pericarditis, surgical intervention such as a pericardiotomy may be required [1, 3].

Post-procedure care focuses on use of nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine to prevent recurrence and effusive-constrictive pericarditis [1]. Regular follow-up with echocardiography is crucial for the continued monitoring for recurrence and treatment effectiveness [5].

ICU Considerations

Diagnosing tamponade in mechanically ventilated patients and post-cardiac surgery presents unique challenges due to dynamic hemodynamic states and potential presence of surgical artifacts. In mechanically ventilated patients the classic cardiac tamponade signs may be mitigated by positive pressure ventilation. Echocardiography remains an essential monitoring tool for guiding diagnosis and management for these unique challenges [2-3].

A multidisciplinary team involving intensivists, cardiologists, and cardiothoracic surgeons is essential for effective cardiac tamponade management. This ensures comprehensive care and collaborative decision-making. This approach leads to accurate diagnoses with advanced imaging techniques and timely procedural or surgical interventions [1-3].

Conclusion

Cardiac tamponade is a life-threatening condition characterized by accumulation of fluid or air in the pericardial space, leading to increased intrapericardial pressure and impaired cardiac filling and potentially obstructive shock [1]. Cardiac tamponade symptoms depend on the acuity of its progression. Echocardiography is essential for diagnosis [2,4]. If left untreated cardiac tamponade can become rapidly fatal. Urgent pericardiocentesis or a surgical pericardiotomy may be indicated depending on severity of symptoms and etiology of the disease [1].

REFERENCES:

1. Adler, Y., Ristic, A. D., Imazio, M., Brucato, A., Pankuweit, S., Burazor, I., . . . Oh, J. K. (2023). Cardiac Tamponade. Nature Review Disease Reviews, 9(36).
2. Kearns, M. J., & Walley, K. R. (2018). Tamponade: Hemodynamic and Echocardiographic Diagnosis. Contemporary Reviews in Critical Care Medicine, 1266-1275.
3. Levitov, A., Frankel, H. L., Blaivas, M., Kirkpatrick, A. W., Su, E., Evans, D., . . . Elbarbary, M. (2016). Guidelines for the Appropriate Use of Bedside General and Cardiac Ultrasonography in the Evaluation of Critically Ill Patiens - Part II: Cardiac Ultrasonography. Critical Care Medicine Medicine, 1206-1227.
4. Roy, C. L., Minor, M. A., Brookhart, M. A., & Choudhry, N. K. (2007). Does This Patient With a Pericardial Effusion Have Cardiac Tamponade? JAMA, 297(16), 1810-1818.
5. Sinnaeve, P., & Adriaenssens, T. (2019). A Contemporary Look at Pericardiocentesis. Trends Cardiovasc Med, 29(7), 375-383.
6. Vakamudi, S., Ho, N., & Cremer, P.C. (2017). Pericardial Effusions: Causes, Diagnosis, and Management. Progress in Cardiovascular Diseases, 59, 380-388.

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