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Cardiac tamponade is a life-threatening condition in which the accumulation of fluid or gas in the pericardial sac prevents adequate filling of the heart and compromises cardiac output. Prompt diagnosis and treatment is imperative if the patient is to survive. Unfortunately, the signs and symptoms can be subtle and easily missed. This is especially true in the intensive care unit (ICU), where mechanical ventilation and sedation can limit physical examination and prevent the patient from vocalizing symptoms. Echocardiography is an important tool in the diagnosis of cardiac tamponade because ultrasound equipment is readily available, portable, and can confirm or refute a clinical diagnosis. The intensivist with the ability to perform a basic cardiac ultrasound has the opportunity to make a timely diagnosis of cardiac tamponade and sometimes even save the life of a critically ill patient.

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The pericardial sac surrounds the heart and is formed by two layers—the outer, pleural pericardium, and the inner, visceral pericardium. Histologically, the pericardium is composed of collagen and elastin fibers that combine to give the structure both its stiffness and elastic quality.1 Normally, the pericardial sac contains 30–50 milliliters (mls) of a low protein, transudative fluid that originates from the visceral pericardium and is thought to act as a lubricant surrounding the beating heart. Typically, the pressure within the pericardial sac is equivalent to the pleural pressure or approximately 5 millimeters of mercury (mm HG) below the central venous pressure.2 Under normal conditions, the pericardium may prevent excessive motion of the heart and reduces friction between moving organs. The pericardium also serves to prevent acute cardiac dilatation and contributes to ventricular interdependence, the mechanism whereby the filling of one ventricle affects the filling of the other. However, cardiac function remains normal in rare individuals with a congenital absence of pericardium.

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Pericardial effusion is defined as an accumulation of fluid in the pericardial sac; this fluid can either be transudative 2° to impaired lymphatic drainage, or more commonly exudative (serous, hemorrhagic, or purulent). On rare occasions, chylous fluid (2° to pancreatitis) or air (2° to esophageal rupture) in the pericardial sac has also been described. The physiologic effects of a pericardial effusion depend on both the amount of fluid and the rate of accumulation (Figure 12.1). When a pericardial effusion accumulates gradually, the compliant pleural pericardium is able to stretch and the pressure in the pericardial sac can remain relatively low until late in the disease course. Accordingly, pericardial effusions of 2 liters have been described in relatively asymptomatic patients with chronic disease. Once the pericardial reserve volume is exhausted, however, small incremental increases in pericardial fluid will result in large increases in pericardial pressure. When pericardial effusions develop rapidly, the pleural pericardium is unable to adapt and the pericardial reserve volume is relatively small. In these cases, very small increases in volume can cause rapid increases in pericardial pressure.3

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