The following symptomatology are observable in patients with cardiac tamponade:

• Dyspnea – This results with the ineffective pulmonary delivery of the blood by the heart. 
• Hypotension – Blood pressure drops with the progressive decrease in the systemic venous return.
• Jugular enlargement – This vein engorges with the increasing jugular venous pressure [3]. 
• Chest wall injuries – These findings are eminent in patients who had undergone chest trauma.
• Tachypnea – This is a compensatory reaction of the lungs to oxygenate the blood in the advent of a decreasing cardiac output. 
• Hepatomegaly – An acute or chronic passive congestion of the liver resulting to enlargement can occur due to the increasing venous pressure. 
• Diminished or muffled heart sounds – This auscultatory finding is observable in cardiac tamponade patients due to the displacement of the heart secondary to the fluid accumulation. 
• Paradoxical pulse (pulsus paradoxus) – The exaggerated pulse is generated due to the abrupt decrease in blood pressure during respiratory inspiration [4]. 
• Kussmaul sign – This sign refer to the increased distention of jugular vein due to the increase in venous pressure during inspiration.
• Dysphoria - This is a restless behavior exhibited by patients with cardiac tamponade as reaction to impending death [5].

Patients presenting with low blood pressure while in cardiac tamponade are unable to exhibit the Kussmaul sign, jugular venous distention, and pulsus paradoxus due to the hypovolemic state of the system. This type of cardiac tamponade is clinically referred to as low pressure tamponade occurring in 20% of all cardiac tamponade cases [6].

The following diagnostic modalities and tests are being implored among patients with cardiac tamponade:

• Chest radiograph – Chest X-ray is routinely done identify the enlarging pericardial sac and isolate chest injuries.
• Computed tomography (CT scan) – CT scan can effectively identify and measure the compression of the coronary sinus which is an early sign of cardiac tamponade [7].
• Echocardiography – The two dimensional echocardiography can identify the obliteration of the spaces between the heart and the visceral side of the pericardium. Echocardiography can accurately measure the volume of fluid accumulation causing the cardiac tamponade. 
• Electrocardiography (ECG) – The 12 leads ECG will exhibit sinus tachycardia, low voltage QRS complexes, PR segment depression, and electrical alterans. This characteristic changes are very typical of cardiac tamponade. 
• Pulse oximetry – This will monitor the level of blood oxygenation and could detect pulsus paradoxus among patients with cardiac tamponade [8]. 
• Cytopathologic studies – In some cases of pericardial effusion, a sample of fluid is being aspirated for laboratory study. This will identify the causative agent of the effusion and may also identify the antibiotic sensitivity of the pathogen [9].

Patients with cardiac tamponade are always treated as a medical emergency. Patients are immediately attached for oxygen inhalation upon admission in the emergency room. Isotonic crystalloids are used to resuscitate the volume loss while the lower extremities are elevated. Inotropic agents like dobutamine is incorporated in the fluids to assists the pumping of the heart. Inpatients are subjected to pericardiocentesis and attached to a close drainage system to drain the reaccumulating fluids. Balloon pericardiotomy may also be instituted to restore the pericardial window. In extreme cases, an open thoracotomy with pericardiotomy is performed to directly drain the fluid and correct any anatomic defects [10].

Cardiac tamponade is a medical emergency. The failure to evacuate the pericardial fluid immediately can result into death. Effusion that gradually accumulates and does not reach a total volume of 150 ml may be averted when the underlying causes is immediately addressed. Penetrating injuries to the chest wall causing cardiac tamponade carry a grim prognosis.

Cardiac tamponade can be caused by several medical conditions. Among these includes:

• Bacterial or viral pericarditis
• Hemorrhage within the pericardium
• Tumor in the vicinity of the heart
• Rupture of the heart muscles
• Blunt trauma to the chest

In the United States, the incidence of cardiac tamponade is estimated to be 2 cases per 10,000 population. Cardiac tamponade is more common in males than females with a ratio of 7:3 in children and 1.25:1 in adults. Traumatic causes and HIV infection are common causation in cardiac tamponade among young adults while renal failure and malignancies are more common in the elderly group.

The basic pathophysiology of cardiac tamponade starts with the accumulation of fluid in the space between the pericardium and the heart. The common fluid accumulation in the pericardial space is usually hemorrhagic, chylous, serous, or serosanguinous in nature. The initial phase of the pericardial effusion increases the filling pressure of the heart ventricles making the ventricles physiologically stiffer. The continuous accumulation of fluid in the pericardial space increase the pericardial pressure beyond the ventricular filling pressure reducing the cardiac output significantly [1].

The progressive loss in functional cardiac output due to the cardiac tamponade diminishes the systemic venous return and consequently results in the collapse of the right atrium and right ventricles. Pericardial effusion as low as 150 ml accumulation can already greatly impede the cardiac output and function [2]. Although pericardial stretching with time can make the myocardium adaptive to this kind of restrictive insults, making the heart function normally and physiologically despite the presence of pericardial effusion.

Chest trauma is one of the leading cause of cardiac tamponade, thus; the prudent use of seatbelts during driving greatly prevents the occurrence of accidental blunt trauma to the chest. Mild septicemia must be promptly treated to avoid the untoward complication of a bacterial or viral pericardial effusion. Patients with history of recurrent effusion in the pericardial space will benefit from the use of sclerosing agents to obliterate the potential space.

Cardiac tamponade occurs when the blood or fluids starts to build up between the myocardium and the pericardium that causes compression of the heart. The restrictive cardiac condition in cardiac tamponade limits the blood flow that is being pumped by the heart. Cardiac tamponade is a life-threatening condition that could be reversed rapidly with prompt and proper therapeutic interventions.

• Definition: Cardiac tamponade is clinically defined as the accumulation of fluid in the pericardial space which alters cardiac filling and cardiac output.
• Cause: Cardiac tamponade is caused by blunt and penetrating injuries to the chest. Tumors, infection, and myocardial rupture can also precipitate cardiac tamponade.
• Symptoms: Cardiac tamponade is heralded by the Beck’s triad of hypotension, distended jugular veins, and distant heart sounds. Other signs of cardiac tamponade includes dyspnea, tachypnea, hepatomegaly, paradoxical pulses, and dysphoria.
• Diagnosis: The diagnosis of cardiac tamponade may be ascertained by the use of chest X-ray, CT scan, 2D echocardiography, ECG, and cytopathologic studies.
• Treatment and follow-up: This medical emergency is initially treated with oxygen inhalation and fluid resuscitation with inotropic agents. A surgical pericardiocentensis is done to drain the pericardial sac with the accumulating fluids. 

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