Cardiac tamponade due to cardiac metastases

Laboratory investigation was significant for a mild decrease of white blood cell count and moderate normocytic normochromic anaemia. Liver function tests were elevated with mild hypoproteinemia and hypoalbuminemia. Cardiac and inflammatory markers were not elevated.

The chest X ray in posteroanterior projection on the day of admission showed enlarged cardiac silhouette (increased cardiothoracic ratio) without pulmonary congestion. Transthoracic echocardiography showed large pericardial effusion of about 500-600 ml with swinging motion of heart, left ventricle was normal in size and systolic function, left atrium, right atrium, and right ventricle were of normal size, mild pulmonary hypertension was detected. Examination also revealed presence of echo contrast masses which were suspicious to be cardiac metastases. One tumor (8x8 mm) was localized in right atrium, the other was behind left atrium (18x6 mm).

Because of clinical, radiological and echocardiographic picture suspicious of cardiac tamponade due to newly diagnosed cardiac metastases the patient was closely monitored with regular checks of vital signs and was parenterally rehydrated. Within a few days, an overall progression of clinical worsening was documented. The patients was severely dyspnoeic, hypotensive, with distention of jugular veins and decreased cardiac tones. Repeated ECG documented normal heart frequency but progression of low voltage of QRS complexes diffusely (Figure 3). Control echocardiography showed persisting swinging heart motion, large pericardial effusion of about 600-700ml with tamponade physiology, patient was indicated for pericardiocentesis and therefore referred to Department of Cardiology of East Slovak Institute of Cardiovascular Diseases.

Cardiac tamponade

Cardiac tamponade is caused by the buildup of pericardial fluid (exudate, transudate or blood) that can accumulate for several reasons. Hemorrhage, such as from a penetrating wound to the heart or ventricular wall rupture after an MI, can lead to a rapid increase in pericardial volume. Other risk factors, which tend to produce a slower growing effusion, include infection (TB, myocarditis), autoimmune diseases, neoplasms, uremia, and other inflammatory diseases (pericarditis). Pericardial fluid that builds up slowly is better tolerated in patients than rapid accumulations - hence traumatic causes (hemopericardium) require small volumes to causes hemodynamic instability versus pericardial effusions from medical causes such as malignancy where large volumes of fluid may accumulate in pericardial sac before patients become symptomatic.

Clinical signs in a patient with cardiac tamponade include tachycardia, hypotension, raised jugular venous pressure, muffled heart sounds. A key diagnostic finding is pulsus paradoxus (conventionally defined as an inspiratory decrease in systolic arterial pressure of 10 mmHg during normal breathing).

The diagnosis of cardiac tamponade can be suspected on history and physical exam findings. An ECG may show signs of pericarditis, with especially low QRS voltages and electrical alternans (Figure 4). Both ECG signs are generally considered to be an expression of the damping effect of pericardial fluid and swinging heart. Chest x-ray may show an enlarged heart (Figure 5) and may strongly suggest pericardial effusion if a prior chest radiograph with normal cardiac silhouette is available for comparison. Echocardiography is the single most useful diagnostic tool to identify pericardial effusion and estimate its size, location and degree of haemodynamic impact.

The treatment of cardiac tamponade involves drainage of the pericardial fluid, preferably by needle pericardiocentesis, with the use of echocardiographic or fluoroscopic guidance, and should be performed without delay in unstable patients. Alternatively, drainage is performed by a surgical approach, especially in some situations such as purulent pericarditis or in urgent situations with bleeding into the pericardium.