Cardiac tamponade is aPHYSOLOGICAL diagnosis.

The gold standard for the diagnosis of cardiac tamponade is the increase in stroke volume AFTER pericardiocentesis -- a retrospective (therapeutic) diagnosis.

In practice, the diagnosis is INFERRED prior to pericardiocentesis:

(a) Presence of a pericardial effusion

(b) Clinical evidence of tamponade physiology

(c) Sonographic inferences of tamponade physiology

The sonographic signs that are suggestive of cardiac tamponade:

Nevertheless, cardiac chamber(s) collapse during diastole is not that easy to time, and trans-valvular flow variation during respiration is not that easy to measure.   These advanced skills will not discussed here.  As to mechanical alternans, it is quite uncommon.

Assessment of the IVC's collapsibility, on the other hand, is more practical: quick to image and informs management in the interim.

It has been demonstrated that IVC plethora in conjunction with a pericardial effusion is highly sensitive (97%) though poorly specific (40%) for cardiac tamponade (JACC 1988;12:1470-7.)in the right clinical context.  This means that an IVC that is exhibiting collapsing >50% with respiratory variation rules out cardiac tamponade physiology.  However, a plethoric IVC is not good enough to definitively rule it

This makes intuitive sense.  In tamponade, the increasing intra-pericardial pressure is transmitted to the  right atrium -- increasing it's pressure.  This increased RA pressure, subsequently, is transmitted to the IVC (provided the patient is not hypovolemic) which raises the central venous pressure.  This elevated CVP is sonographically reflected via the diminishing collapsibility of the IVC.

Here we have a large pericardial effusion imaged from the subcostal view.  The IVC exhibiting respiratory collapsibility.  This patient was, in fact, hemodynamically stable with no clinical or investigatory signs of end-organ hypoperfusion.  This really illustrates the point that a large effusion does not equate to tamponade.

Here we have a patient who was asymptomatic and hemodynamically stable just prior to a routine hemodialysis session where the patient's blood pressure precipitously dropped whenever venous siphoning commenced.  This patient, also, exhibited a large pericardial effusion and collapsing IVC. 

During dialysis, central venous pressure reduces.  This would result in the intra-pericardial pressure exceeding diastolic chamber pressure (in particular, the right atrial pressure) which would impair diastolic filling and, therefore, reducing stroke volume.

The patient was NOT in tamponade, but it was precipitated during dialysis.

In this situation, it is called low pressure tamponade. (Circulation. 2006;114:945-952.)  This is the exception to the rule illustrated above.

In this case, pericardiocentesis was performed so that the patient may tolerate the hemodynamic perturbance of dialysis.