Cardiac tamponade pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S. Ramyar Ghandriz MD[3]

Overview

Cardiac tamponade occurs when the pericardial space fills up with fluid faster than the pericardial sac can stretch. If the amount of fluid increases slowly (such as in hypothyroidism) the pericardial sac can expand to contain a liter or more of fluid prior to tamponade occurring. If the fluid occurs rapidly (as may occur after trauma or myocardial rupture) as little as 100 ml can cause tamponade.[1]

Pathophysiology

Anatomy and Physiology of Pericardium

Layers of the Pericardium

  • The pericardium is made up of two layers:
    • Fibrous pericardium
      • Hard protective external layer
      • Attached to sternum anteriorly by sterno-pericardial ligaments and fused with the central tendon of the diaphragm and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
    • Serous pericardium
      • Smooth internal layer made up of 2 components:
        • Parietal: reflects onto fibrous pericardium
        • Visceral: reflects onto heart and great vessels and forms the epicardium, the external layer of the heart wall
  • Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.[2][3][4]

Pericardial Sinuses

  • There are two small chambers or sinuses located where the visceral and parietal pericardia are continuous with one another within the pericardial cavity.
  • Transverse sinus:
    • Located posterior to the pulmonary trunk and ascending aorta at the level between the superior vena cava and aortic arch
    • Formed after dorsal mesocardium rupture embryonically
    • Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac systole
    • Utilized surgically to pass surgical clamps or place ligatures around great arteries.
  • Oblique sinus:

Pathogenesis

The outer pericardium is made of fibrous tissue [8] which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase [9].

Ordinarily, drainage from the pericardium occurs via the thoracic duct and the right lymphatic duct into the right pleural space. In the absence of disease, the normal pericardium contains only 20-50 cc of serous fluid due to ultrafiltration from the blood. Up to about 75 cc can accumulate acutely in the pericardium without hemodynamic compromise. Much greater amounts of fluid can accumulate chronically over a prolonged period of time as the pericardial sac stretches slowly to accommodate the fluid without hemodynamic compromise. However, if the volume of the fluid accumulation is too rapid and or large, then the hemodynamic compromise can occur with a rise in pericardial pressure. This in turn reduces stroke volume, and eventually, cardiac output.

If fluid continues to accumulate, then with each successive diastole, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to a decreased stroke volume [10]. This causes obstructive shock to develop, and if left untreated, cardiac arrest may occur (in which case the presenting rhythm is likely to be Pulseless electrical activity).

Below is a video demonstrating hemorrhagic effusion leading to cardiac tamponade. {{#ev:youtube|QwgfuDegC5Y}}

Gross Pathology

References

  1. *Fornauer, Andrew (2003). "Pericardial Tamponade Complicating Central Venous Interventions". Journal of Vascular and Interventional Radiology. PMID 12582195. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  2. Kishore, K. (2003). The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump. J Postgrad Med, 49:282-4.
  3. Moore, K. L., Agur, A. M., & Dalley, A. F. (2011). Essential Clinical Anatomy - Fourth Edition. Lippincott Williams & Wilkins.
  4. Tank, P. W. (2009). Grant's Dissector - Fourteenth Edition. Lippincott Williams & Wilkins.
  5. Kishore, K. (2003). The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump. J Postgrad Med, 49:282-4.
  6. Moore, K. L., Agur, A. M., & Dalley, A. F. (2011). Essential Clinical Anatomy - Fourth Edition. Lippincott Williams & Wilkins.
  7. Tank, P. W. (2009). Grant's Dissector - Fourteenth Edition. Lippincott Williams & Wilkins.
  8. Thibodeau, G.A., Patton, K.T. (2000). Anatomy & Physiology. Missouri: Mosby ISBN 9780323010962
  9. Mattson Porth, C. (Ed.) (2005) (7th Ed.) Pathophysiology: Concepts of Altered Health States. Philadelphia : Lippincott Williams & Wilkins ISBN 978-0781749886
  10. Mattson Porth, C. (Ed.) (2005) (7th Ed.) Pathophysiology: Concepts of Altered Health States. Philadelphia : Lippincott Williams & Wilkins ISBN 978-0781749886

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