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- Accurate hemodynamic assessment of seriously ill patients requires an understanding of the concepts of transmural (effective) filling pressures and ventricular interaction.
- A systematic approach to the assessment of a patient with a low cardiac output and increased right atrial pressure will result in the correct determination when pericardial disease is a contributing factor.
- Echocardiography is the most important test for the initial evaluation of patients with pericardial disease.
- Pericardial drainage should be performed without delay in patients with cardiac tamponade. Volume loading or inotropic agents are not effective therapies for tamponade.
- Conditions such as localized tamponade and constrictive pericarditis must be considered in patients without a good alternative explanation for low cardiac output.
- Although rare, the possibility of purulent pericarditis should be considered in patients who are most susceptible.
- Anticoagulation is not contraindicated in pericarditis.
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A pericardial cause of otherwise unexplained low cardiac output should always be considered in critically ill patients. Pericardial inflammation or infection may also deserve consideration. This chapter focuses largely on the hemodynamic implications of constraint to ventricular filling and the approach to diagnosis and treatment of pericardial disease. The goals are to provide the reader with tools to assess the potential for suspected or known pericardial disease to relieve a patient's condition. The reader should refer to standard cardiology texts to learn the details of specific causes of pericardial disease (Table 28-1).
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Pericardial Constraint
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The key to understanding pericardial physiology is to understand transmural pressure. The ventricles distend in proportion to transmural pressure, not to intracavitary pressure; this is frequently overlooked because changes in intracavitary pressure often (but not always) reflect changes in transmural pressure. Effective distending pressure is the pressure difference across the chamber wall, that is, transmural pressure.1 This principle is rarely important with respect to systolic pressures2 but may be critical with respect to diastolic pressures.3 If left ventricular end-diastolic pressure (LVEDP) is 12 mm Hg, then LVEDP is 12 mm Hg greater than atmospheric pressure. However, if pericardial pressure is 4 mm Hg, then transmural LVEDP, the effective distending pressure, is 8 mm Hg. Further, if LVEDP increases to 15 mm Hg and pericardial pressure increases to 7 mm Hg, then transmural LVEDP remains 8 mm Hg and left ventricular end-diastolic volume (LVEDV) does not change.
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Ventricular Interaction
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