Cardiac tamponade is the result of accumulation of fluid, pus, blood, gas, or benign or malignant neoplastic tissue within the pericardial cavity, which can occur either rapidly of gradually over time, but eventually results in impaired cardiac output.
This is to be distinguished from a pericardial effusion, which can be very large but does not necessarily impair cardiac function.
Pulsus paradoxus is an exaggerated fall in systolic blood pressure of 10 mm Hg or more during inspiration. This is one of the most useful physical findings and an ominous sign of impending hemodynamic collapse, but again it is nonspecific and may be blunted, absent, or difficult to reproduce.
The Beck triad consists of muffled heart sounds, hypotension, and jugular venous distention. It strongly suggests tamponade but is present in only a minority of patients.
Tamponade results from the incremental increase in the intrapericardial volume which raises the intrapericardial pressure. This pressure is transmitted to the cardiac chambers with both reduced intracardiac volume and increased resistance to filling with resultant severe hemodynamic impairment and eventually reduced cardiac output.
Rate of accumulation is more significant in establishing cardiac tamponade than the ultimate size or composition of the pericardial contents. Acute or rapidly developing pericardial effusions can abruptly increase the intrapericardial pressure and produce cardiac tamponade with as little as 100-200 mL of pericardial fluid.
Chest radiographs may show cardiomegaly with or without an epicardial fat pad sign suggesting a pericardial effusion.
In patients with tamponade due to pneumopericardium, termed tension pneumopericardium, a substantial decrease in the size of the cardiac silhouette may be observed on radiographs, the small heart sign.
Echocardiography is considered the gold standard, and commonly first line, imaging modality for assessment of cardiac tamponade. This is due to its ability to provide detailed structural and functional information about the heart, pericardium and inferior vena cava (IVC). It also allows approach planning for pericardiocentesis.
Information that can be detected using echocardiography includes:
- size and location of pericardial effusion
- the presence or absence of loculated pericardial effusion
- evidence of hemodynamic compromise, including
- right atrial collapse
- right ventricular diastolic collapse
- respiratory inflow variation across the mitral and tricuspid valves
- assessment of the IVC (fixed and unreactive in tamponade)
However, in equivocal cases or when echocardiography is not feasible, additional imaging studies including computed tomography or magnetic resonance are necessary.
CT provides valuable information about the possible nature of pericardial effusions based on the attenuation measurements of the collection.
Some of the reported CT findings in tamponade include (nonspecific findings):
- superior vena cava enlargement
- diameter similar to or greater than that of the adjacent thoracic aorta
- inferior vena cava enlargement
- diameter greater than twice that of the adjacent abdominal aorta
- hepatic and renal vein enlargement
- periportal edema
- reflux of contrast material
- into the IVC
- into the azygos system
- compression of the coronary sinus 2
- angulation or bowing of the interventricular septum
MRI has a limited role in the setting of cardiac tamponade owing to the emergent and life-threatening nature of this condition. Nevertheless, MRI can provide information useful in characterizing the nature of the pericardial effusion in addition to the effects on cardiac functioning and diastolic filling.
Treatment and prognosis
Treatment involves the expedient drainage of the pericardial collection and, where feasible, repair or treatment of the underlying cause. This can be performed percutaneously with either landmark or ultrasound guided pericardiocentesis, via open sternotomy or increasingly with a balloon pericardiotomy.