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Cardiac tamponade, also known as pericardial tamponade, is an emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If the fluid significantly elevates the pressure on the heart it will prevent the heart’s ventricles from filling properly. This in turn leads to a low stroke volume. The end result is ineffective pumping of blood, shock, and often death.
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]
Causes of increased pericardial effusion include hypothyroidism, physical trauma (either penetrating trauma involving the pericardium or blunt chest trauma), pericarditis (inflammation of the pericardium), iatrogenic trauma (during an invasive procedure), and myocardial rupture.
Cardiac tamponade is caused by a large or uncontrolled pericardial effusion, i.e. the buildup of fluid inside the pericardium.[2] This commonly occurs as a result of chest trauma (both blunt and penetrating),[3] but can also be caused by myocardial rupture, cancer, uraemia, pericarditis, or cardiac surgery,[2] and rarely occurs during aortic dissection,[4] or whilst the patient is taking anticoagulant therapy.[5] The effusion can occur rapidly (as in the case of trauma or myocardial rupture), or over a more gradual period of time (as in cancer). The fluid involved is often blood, but pus is also found in some circumstances.[2]
Myocardial rupture is a somewhat uncommon cause of pericardial tamponade. It typically happens in the subacute setting after a myocardial infarction (heart attack), in which the infarcted muscle of the heart thins out and tears. Myocardial rupture is more likely to happen in elderly individuals without any previous cardiac history who suffer from their first heart attack and are not revascularized either with thrombolytic therapy or with percutaneous coronary intervention or with coronary artery bypass graft surgery.[6]
The outer pericardium is made of fibrous tissue[7] which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase.[2]
If fluid continues to accumulate, then with each successive diastolic period, 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 decreased stroke volume.[2] This causes obstructive shock to develop, and if left untreated then cardiac arrest may occur (in which case the presenting rhythm is likely to be pulseless electrical activity)
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