A 37-year old man presents to his primary care physician concerned about multiple episodes of dizziness associated with palpitations. He is unable to exert himself in his activities of daily living. His past medical history is significant for hyperlipidemia, anxiety, gastroesophageal reflux disease, occasional migraines, lower back pain, and constipation. He had an appendectomy at age 12, but otherwise, no surgical history. He has an allergy to bananas and latex. His medications include simvastatin, lorazepam, esomeprazole, naproxen, and colace. He smokes one pack of cigarettes per day. He does not consume alcohol and has never tried taking recreational drugs. On physical exam he is found to be bradycardic at 42 beats per minute. His blood pressure is 110/65, respiratory rate 16 breaths per minute, and oxygen saturation 98% on room air. His lungs exam is remarkable for mild rales at the bases bilaterally and he has 2+ edema in his lower extremities. His ECG shows complete heart block. After medical optimization of his heart failure symptoms, he presents to an interventional cardiologist for pacemaker placement. During the pacemaker placement, which was performed under sedation, the patient moves on the procedure table as the first lead was being placed. He then becomes suddenly dyspneic and increasingly hypotensive. His blood pressure is 80/45, heart rate 110 beats per minute, respiratory rate 25 breaths per minute and pulse oximetry 98%. Pericardial tamponade is suspected.

Cardiac tamponade is defined as pathologic fluid in the pericardial space leading to a restriction in ventricular filling and subsequently a decrease in cardiac output. Normally, the pericardial sac contains 20–50 mL of serous fluid that mitigates the force of friction on the epicardium. Cardiac tamponade occurs when the reserve volume of the pericardial sac is exceeded by filling with blood, clot, gas, fluid, or pus [1]. The physiology of cardiac tamponade is less a function of the effusion’s composition and more a function of the rate at which it accumulates. There are four generally accepted categories of cardiac tamponade. Acute cardiac tamponade usually occurs within minutes and is most often secondary to hemopericardium from trauma. It occurs when blood accumulates more rapidly than the pericardial sac can accommodate. In severe cases, this can lead to complete collapse of the right atrium and/or the right ventricle. Subacute cardiac tamponade most often occurs over days to weeks due to large effusions, which accumulate more slowly, often from idiopathic or neoplastic causes. Low pressure cardiac tamponade is a special case when pericardial effusion and hypovolemic shock coexist. Due to the fact that ventricular pressures are low, the pressure gradient across the myocardium may be large even with relatively low pericardial pressures [2]. Finally, regional tamponade develops when a loculated effusion or hematoma exerts pressure across the myocardium. This is more difficult to diagnose on physical exam because typical findings are absent due to a focal source of compression [3].

Cardiac tamponade arises from a number of causes including infectious, noninfectious and autoimmune origins. While acute idiopathic pericarditis is the leading cause of tamponade worldwide, it is proportionately much more common in patients with tuberculous, neoplastic, or purulent pericarditis [4]. A large prospective series evaluated the etiologies of primary acute pericarditis [5]. Nearly half had acute idiopathic pericarditis, and the remaining patients commonly had metastatic disease and tuberculous pericarditis. Infectious causes of tamponade can be divided into viral, bacterial, fungal and parasitic causes. Coxsackie, echovirus and adenovirus are common viral causes, while Staphylococcus, Streptococcus, pneumococcus, and tuberculosis are the most common bacterial causes [6]. Fungal causes include Histoplasmosis, aspergillosis, and coccidioidomycosis, and the most common parasitic causes are echinococcus and toxoplasmosis. Metastatic lung and breast cancer, Hodgkin’s lymphoma and melanoma are the most common sources of malignant effusions. Primary cardiac causes are comprised of early infarction pericarditis, post-pericardiotomy syndrome, dissecting aneurysms and myocarditis. Tamponade can be induced by blunt and penetrating trauma like, and it can occur as a complication of cardiac catheterization and pacemaker placement. Rheumatologic causes, include SLE and vasculitis, and occur secondary to inflammation. Uremia is a common metabolic cause. Any process which leads to an effusion, particularly if large or rapidly accumulating, can induce tamponade physiology.

Physical exam findings of a patient with pericardial tamponade are sinus tachycardia, jugular venous distension, and pulsus paradoxus. Secondary signs of pericarditis include muffled heart sounds and rub. Dyspnea (sensitivity 87–89%), tachycardia (sensitivity 77%), pulsus paradoxus (sensitivity 82%), and elevated JVP (sensitivity 76%) are most useful in their negative predictive value [7]. That is, they are useful for ruling out tamponade when absent. If a patient has pulsus paradoxus, the odds of having tamponade increase threefold, and if absent, the odds of having tamponade are reduced 30-fold.

Pulsus paradoxus is an exaggeration of a normal decrease in systolic blood pressure, which occurs during inspiration [8]. Under conditions of increased pericardial pressures, changes in right and left ventricular volume inevitably affect each other, as there is no additional reserve volume in the pericardial sac. At least three mechanisms have been proposed to explain this phenomenon [9]. With inspiration, increased negative pressure in the intrathoracic cavity increases venous return to the right side of the heart. The increased preload, in turn, causes bulging of the septal wall into the left ventricle, decreasing end-diastolic left ventricular volume. This exemplifies ventricular interdependence. Increased compliance of pulmonary vasculature also occurs during inspiration, leading to pooling in the pulmonary circulation. Finally, the increase in negative intrathoracic pressure opposes contraction of the left side of the heart, leading to increased afterload. These three forces conspire to decrease systolic blood pressure. Kussmaul’s sign describes the disappearance of the peripheral pulse with inspiration, which is caused by the drop in blood pressure described above.

The diagnostic criteria for cardiac tamponade are not well defined. It is generally diagnosed when both a pericardial effusion and hemodynamic compromise are present. Another commonly used definition is one which can only be made retrospectively: the presence of a pericardial effusion as seen by either transthoracic or transesophageal echocardiography and hemodynamic compromise that is relieved by pericardial fluid drainage [10].

While many techniques may be helpful in diagnosing pericardial effusion, establishing the diagnosis of tamponade physiology on the basis of noninvasive testing is challenging. EKG is the first test often performed. PR segment depression, low voltage QRS complex, and electrical alternans are EKG findings that are specific but not sensitive for pericardial effusion [11]. Overall, EKG has a low sensitivity for diagnosing pericardial effusion and cardiac tamponade.

Transthoracic echocardiogram (TTE) clearly demonstrates the presence or absence of effusion. A study by Merce et al. prospectively assessed patients with moderate to large pericardial effusions over a 2-year period for tamponade [12]. They found that collapse of one or more right cardiac chambers was highly sensitive for tamponade, while abnormal venous flow pattern by Doppler was more specific—systolic over diastolic predominance, respiratory accentuation of this difference and expiration inversion of the diastolic component. Other TTE signs of tamponade include exaggerated inspiratory variation of the right and left ventricle, collapse of any chamber, IVC plethora and abnormal reduction in flow across the mitral and aortic valves during inspiration [13].