CHAPTER 20 Eric M. Crespo, Sidney C. Smith and George A. Stouffer Effusive–constrictive pericarditis is an uncommon syndrome characterized by constriction of the heart by the visceral pericardium in the presence of a tense pericardial effusion. In these patients, pericardiocentesis converts the hemodynamics from those typical of tamponade to those of constriction. It is diagnosed when elevated right atrial pressures persist despite reduction of intrapericardial pressures to normal levels by pericardiocentesis. Although first observed in the 1960s [1], it was not well described until the publication of a 13‐patient case series by Hancock in 1971 [2]. Since that time there has been a paucity of medical literature on the topic, and it was not until the recent publication of a case series by Sagrista‐Sauleda that more complete information about the etiology, incidence, and prognosis of effusive–constrictive pericarditis became known [3]. In their series, Sagrista‐Sauleda and colleagues prospectively evaluated 1184 patients presenting to their institution with pericarditis of any type over a 15‐year period. Based on their data, the authors estimate that the prevalence of effusive–constrictive pericarditis is approximately 1.3% of all patients with pericarditis and 6.8% of patients with clinical tamponade. Additionally, they found that although effusive–constrictive pericarditis can occur with all types of pericarditis, it is relatively more frequent with radiation‐related pericardial disease and less often associated with postsurgical pericarditis. Other studies have shown a relatively higher frequency with tuberculous pericarditis [4]. The etiology and incidence, however, will likely vary between institutions and between different parts of the world based on the most common causes of pericarditis in each location. The majority of patients diagnosed with effusive–constrictive pericarditis will progress to chronic constriction, but a proportion of those with idiopathic disease may have only temporary cardiac constriction and then go on to eventual full resolution [3,5]. Patients tend to have a subacute presentation and are often initially believed to have cardiac tamponade. The true diagnosis can only be made after constrictive physiology persists despite normal pericardial pressures. Thus, continuous monitoring of intracardiac filling pressures during pericardiocentesis is required to arrive at the correct diagnosis. The hallmark of effusive–constrictive pericarditis is the persistence of elevated right atrial pressure after intrapericardial pressure has been reduced to normal levels by pericardiocentesis. As in both constrictive pericarditis and cardiac tamponade, the expansion of the cardiac chambers during diastole is limited and there are elevation and equalization of diastolic pressures in the atria and ventricles. Prior to drainage of the effusion, the predominant hemodynamic findings are those of cardiac tamponade with a preserved X descent and an absent or attenuated Y descent on the right atrial pressure tracing. Once the effusion has been drained, constrictive physiology predominates, with return and exaggeration of the Y descent leading to a classic M‐ or W‐shaped configuration of the right atrial pressure waveform. The ventricular pressure tracings demonstrate the square root sign due to rapid ventricular filling in early diastole. In a study of 68 patients with tuberculous pericarditis, Ntsekhe et al. found that 36 patients (53%) had effusive–constrictive physiology as defined by these hemodynamic findings during combined pericardiocentesis and cardiac catheterization: (a) mean pericardial pressure of >8 mm Hg prior to fluid removal; (b) difference between right atrial pressure and intrapericardial pressure of ≤4 mm Hg; (c) mean pericardial pressure of 0 ± 4 mm Hg after pericardiocentesis; and (d) mean right atrial pressure of ≥11 mm Hg or failure to decrease by 50% or more of the pre‐pericardiocentesis level [4]. They found that patients with effusive‐constrictive pericarditis were younger, had a higher pre‐pericardiocentesis right atrial pressure, and higher serum and pericardial fluid levels of interleukin‐10. For detailed descriptions of the hemodynamic principles and findings of constrictive pericarditis and cardiac tamponade, refer to Chapters 18 and 19. The findings on initial physical examination are similar to those for a patient presenting with cardiac tamponade. Patients will have elevated jugular venous pressure (JVP), and careful examination of the neck veins may reveal a prominent X descent and an absent Y descent. Kussmaul’s sign, an increase in central venous pressure with inspiration, may be present and manifest as either increased or unchanged (i.e., failure to decrease) JVP during inspiration. Other sequelae of elevated right heart pressures may be noted, including hepatomegaly, ascites, and peripheral edema. Arterial pulsus paradoxus (inspiratory decrease in systolic pressure by ≥10 mm Hg) may also be noted. Additionally, a pericardial friction rub or pericardial knock may sometimes be auscultated. It should be kept in mind, however, that the sensitivity and specificity of different physical examination findings are not well defined. A discussion of pericardial imaging can be found in Chapter 18. It is possible that pericardial calcification may be less common among patients with effusive–constrictive pericarditis than it is among those with strictly constrictive disease. In the series by Sagrista‐Sauleda and colleagues, none of the patients with effusive–constrictive pericarditis was noted to have pericardial calcification on radiographic examination [3]. As with the hemodynamic findings during catheterization, the echocardiographic findings will fall somewhere on a spectrum between the findings of cardiac tamponade and those of constriction, depending on whether the effusion has been drained and intrapericardial pressure has normalized. Refer to Chapters 18 and 19 for further discussion of the echocardiographic findings in constrictive pericarditis and cardiac tamponade.
Effusive–constrictive pericarditis
Hemodynamics of effusive–constrictive pericarditis
Physical examination
Pericardial imaging techniques
Findings on echocardiography
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