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Cardiac tamponade is a life-threatening condition in which fluid accumulation in the pericardial sac exerts pressure on the heart, leading to impaired ventricular filling, decreased stroke volume, and ultimately hemodynamic collapse.
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It is the hemodynamic consequence of a pericardial effusion, not just the presence of fluid.
https://www.youtube.com/watch?v=PMqeYZ4voks&pp=wgIGCgQQAhgB
https://www.youtube.com/watch?v=9FgpLaCi_KE
| Category | Examples |
|---|---|
| Traumatic | Penetrating injury, post-surgical, catheter perforation |
| Malignant | Lung, breast, lymphoma, leukemia |
| Infectious | Viral (Coxsackie), TB, bacterial |
| Autoimmune | SLE, rheumatoid arthritis |
| Metabolic | Uremia (chronic renal failure), hypothyroidism |
| Iatrogenic | Post-pericardiotomy, post-catheterization |
| Hemorrhagic | Aortic dissection rupture into pericardium, anticoagulation-related bleeds |
Anatomical changes to the heart during cardiac tamponade: a, Schematic of the heart depicting the layers of the pericardium and excessive intrapericardial pressure during cardiac tamponade. b, The basic pathogenetic mechanisms of cardiac tamponade. Progressive intrapericardial accumulation of fluid leads to increased intrapericardial pressure and compression of the heart. Diastolic filling and cardiac output are subsequently impaired, resulting in haemodynamic compromise, circulatory shock and, eventually, cardiac arrest. Owing to ventricular interdependence, expansion of the right ventricle during inspiration compresses the left ventricle, resulting in decreased filling and a drop in stroke volume with a decrease in systolic blood pressure (pulsus paradoxus). During expiration, the left ventricle is filled by the restoration of pulmonary venous return but the right ventricle is compressed and systemic venous return is interrupted.
Prabhakar, Y. et al. Pericardial decompression syndrome: a comprehensive review. World J. Cardiol. 11, 282–291 (2019). Adler, Y., Ristić, A.D., Imazio, M. et al. Cardiac tamponade. Nat Rev Dis Primers 9, 36 (2023). https://doi.org/10.1038/s41572-023-00446-1
Pressure–volume curves depicting acute and chronic pericardial effusion: a, Rapid fluid accumulation in iatrogenic acute pericardial effusion due to, for example, perforation of coronary arteries during percutaneous coronary intervention, myocardial perforation during endomyocardial biopsy or pacemaker lead placement, electrophysiology procedures or trauma. When the effusion reaches the maximum pericardial reserve volume, any further increase in fluid and, consequently, in the rate of expansion will exceed the limit of pericardial stretch. b, Slow fluid accumulation in chronic pericardial effusion. Pericardial stretching over an extended period of time results in a shift in the pressure–volume curve to the right (stress relaxation). Therefore, slowly developing effusions might not necessarily result in cardiac tamponade.
Imazio, M. & Adler, Y. Management of pericardial effusion. Eur. Heart J. 34, 1186–1197 (2013).
Electrocardiogram (ECG):