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Pericardial Effusion and Tamponade

The pericardium is composed of visceral and parietal components. The visceral pericardium is a serosal monolayer that adheres firmly to the epicardium, reflects over the origin of the great vessels, and together with a tough, fibrous parietal layer, envelops the heart10. The pericardial space enclosed between the two serosal layers normally contains up to 50 mL of plasma ultrafiltrate, and a pericardial effusion is considered to be present when accumulated fluid within the sac exceeds this amount10. Cardiac tamponade is characterized by hemodynamic instability due to heart compression by accumulation of fluid, blood, clots, or gas in the pericardial space1.

The pericardium may be affected by all categories of diseases, including infectious, autoimmune, neoplastic, iatrogenic, traumatic, and metabolic1. Pericardial effusions may develop rapidly (acute) or more gradually (subacute, when less than 3 months; or chronic, when longer than 3 months)10. If fluid accumulation is gradual, pericardial pressure remains low because the pericardium can increase its compliance by undergoing stretch, which is accomplished by an increase in surface area and mass5. With continued accumulation of fluid, the intrapericardial pressure eventually increases and becomes high enough to impede cardiac filling—at which time, cardiac function becomes impaired and cardiac tamponade can be considered to be present10.

The true incidence of cardiac tamponade is difficult to estimate, but pericardial diseases likely to progress to tamponade include some infectious diseases (e.g., human immunodeficiency virus infection or tuberculosis), malignancies, renal failure, trauma/iatrogenic, and hemopericardium in aortic dissection and rupture of the heart after acute myocardial infarction12. At postmortem, cardiac tamponade is most often related to hemopericardium, attributable to either ruptured acute myocardial infarction or dissecting aortic aneurysm14.

Pericardial effusions are often discovered incidentally during evaluation of other cardiopulmonary diseases; indeed, the majority of patients have no symptoms specific to the effusion10. Electrocardiography may show signs of large pericardial effusion, with especially low QRS voltage and electrical alternans4, which is an electrocardiographic phenomenon defined as an alternating amplitude or axis of the QRS complexes in any or all leads. Less commonly, compression of the adjacent intrathoracic structures results in hoarseness, hiccough, and nausea1.

Cardiac tamponade often presents as a cardiogenic obstructive shock with shortness of breath, tachycardia, hypotension with a narrow pulse pressure (but blood pressure may be preserved in some cases)2, and pulsus paradoxus (an inspiratory fall of systolic blood pressure of more than 10 mmHg during normal spontaneous breathing), which is an important diagnostic finding in CT7. Jugular venous distention, marked hypotension, and muffled heart sounds (Beck’s triad) are the three classic signs of cardiac tamponade.

Echocardiography is the main diagnostic method for detection of pericardial effusion and tamponade4. The transthoracic approach is often sufficient, but the transesophageal route must be preferred in intubated patients following trauma or cardiac surgery in whom loculated or extrapericardial tamponade may result in nonspecific clinical presentation9. The main echocardiographic sign of cardiac tamponade is heart collapse. It mainly occurs in low pressure cardiac chambers with thin walls—namely the right atria at end diastole (early sign, very sensitive, but poorly specific unless sustained at least one-third of the cardiac cycle)8, and the right ventricle outflow tract at early diastole (late sign, very specific)3; left atrium and left ventricle collapses are less common because intra-cavitary pressures are higher4. The heart collapse is enhanced during the spontaneous expiratory phase, because of the decreased venous return; conversely, it may be mitigated by hypervolemia, pulmonary hypertension, and right ventricle hypertrophy13.

Two of the most common treatments for severe pericardial effusion and cardiac tamponade are pericardiocentesis and pericardiectomy. The choice between the two are based on patient presentation, severity, and provider comfort and experience. Pericardiocentesis can be performed under fluoroscopic or echocardiographic guidance10. Real-time echocardiography guidance with microbubbles injection can be used by experienced staff for safe bedside pericardiocentesis15. In the largest published series, the para-apical location was utilized in two-thirds, while the subxiphoid location was ideal in only 15%11. In an emergency, a blind approach has been used to successfully perform a pericardiocentesis when ultrasound was not available.

Surgical pericardiectomy and drainage, though less commonly performed than pericardiocentesis, is often preferred when the pericardial effusion has reaccumulated or is loculated, biopsy of the pericardium is desired, or the patient has a coagulopathy10. Surgical drainage is preferable in some cases like purulent pericarditis or bleeding (e.g., type A aortic dissection, ventricular free wall rupture)12. In some patients presenting with cardiac tamponade and large pleural effusion, drainage of the pleural effusion may be given priority6.

Despite substantial progress in the detection, quantification, characterization, management, and prognosis of pericardial diseases, and the recent guidelines and recommendations, there is only limited evidence-based data to guide the management of pericardial effusion and cardiac tamponade10. Echocardiography remains critical for recognition and management of pericardial effusions and their hemodynamic sequelae, but when complex effusions are present or echocardiographic imaging is suboptimal, multimodality imaging is essential10.


References

  1. Adler Y, Charron P, Imazio M et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC) Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015;36:2921–2964. https://doi.org/10.1093/eurheartj/ehv318
  2. Argulian E, Herzog E, Halpern DG, Messerli FH. Paradoxical hypertension with cardiac tamponade. Am J Cardiol 2012;110:1066–1069. https://doi.org/10.1016/j.amjcard.2012.05.042
  3. Armstrong WF, Schilt BF, Helper DJ et al. Diastolic collapse of the right ventricle with cardiac tamponade: an echocardiographic study. Circulation 1982;65:1491–1496
  4. Dessap, A.M. & Chew, M.S. Cardiac tamponade. Intensive Care Medicine 2018;44:936-939. http://doi.org/10.1007/s00134-018-5191-z
  5. Freeman GL, LeWinter MM. Pericardial adaptations during chronic cardiac dilation in dogs. Circ Res. 1984;54:294–300.
  6. Furst B, Liu C-JJ, Hansen P, Musuku SR. Concurrent pericardial and pleural effusions: a double jeopardy. J Clin Anesth 2016;33:341–345. https://doi.org/10.1016/j.jclinane.2016.04.056
  7. Gauchat HW, Katz LN. Observations on pulsus paradoxus (with special reference to pericardial effusions): I. Clinical. Arch Intern Med 1924;33:350–370. https://doi.org/10.1001/archinte.1924.00110270071008
  8. Gillam LD, Guyer DE, Gibson TC et al. Hydrodynamic compression of the right atrium: a new echocardiographic sign of cardiac tamponade. Circulation 1983;68:294–301. https://doi.org/10.1161/01.CIR.68.2.294
  9. Grumann A, Baretto L, Dugard A et al. Localized cardiac tamponade after open-heart surgery. Ann Thorac Cardiovasc Surg 2012;18:524–529. https://doi.org/10.5761/atcs.oa.11.01855
  10. Hoit, B.D. Pericardial effusion and cardiac tamponade in the new millennium. Current Cardiology Reports 2017;19(57);DOI 10.1007/s118886-017-0867-5.
  11. Imazio M, Belli R, Beqaraj F, et al. Drainage or Pericardiocentesis alone for recurrent nonmalignant, nonbacterial pericardial effusions requiring intervention: rationale and design of the DROP trial, a randomized, open-label, multicenter study. J Cardiovasc Med. 2014;15:510–4.
  12. Risti AD, Imazio M, Adler Y et al. Triage strategy for urgent management of cardiac tamponade: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2014;35:2279–2284. https://doi.org/10.1093/eurheartj/ehu217/
  13. Santamore WP, Heckman JL, Bove AA. Right and left ventricular pressure-volume response to elevated pericardial pressure. Am Rev Respir Dis 1986;134:101–107. https://doi.org/10.1164/arrd.1986.134.1.101
  14. Swaminathan A, Kandaswamy K, Powari M, Mathew J. Dying from cardiac tamponade. World J Emerg Surg 2007;2:22. https://doi.org/10.1186/1749-7922-2-22
  15. Tsang TSM, Enriquez-Sarano M, Freeman WK et al. Consecutive 1127 therapeutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. Mayo Clin Proc 2002;77:429–436. https://doi.org/10.4065/77.5.429