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Chapter 6
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Pathophysiology ofChronic Constrictive
Pericarditis
The precise pathogenesis of chronic constrictive pericarditis remains conjectural.
Much of the limited evidence gathered from small case series alludes to progression
of an acute pericarditis from a dry stage through an effusive, absorptive, and constrictive phase sequentially, or it may result from a smouldering brosis with no
previous history of acute pericarditis [9, 16–22, 36, 45–55, 66–70]. The factors
responsible for resolution of inammation or its progression to severe brosis
remain conjectural. In large multicentric studies, tubercular pericardial effusion
resolved without constriction in half of the patients, while the rest developed chronic
constrictive pericarditis despite adequate anti-tubercular treatment and steroids [16,
23, 60]. The virtual absence of constrictive pericarditis following rheumatic fever
and its low incidence in tubercular pericarditis in HIV positive patients are noteworthy [16, 19–26, 41, 52–54]. Little research has been done to unravel the inammatory repertoire of pericardial tissue [31]. It appears that tubercular pericarditis is a
hypersensitivity reaction to antigens such as tuberculoproteins. The increased production of interferon-gamma, tumor necrosis factor-alpha, interleukin-1 and interleukin- 2in tubercular pericardial uid suggests that the inammation is orchestrated
by T-helper-1 lymphocytes [10–12]. T-lymphocytes and activated macrophages
probably play an important role in granuloma formation and brosis [29, 30, 38,
52]. Adenosine deaminase, a marker of leukocyte activation, has been associated
with increased numbers of pericardial neutrophils and lymphocytes as well as granulomatous pericardial histology [31–34, 37, 42–44].
Patients presenting in effusive stage, increased duration of illness before presentation, clinical features of cardiac compression, pericardial thickening, and brous
strand on echocardiography and biopsy have all been correlated with subsequent
constriction [13–15, 19–25, 29, 31–33, 35, 45, 66–72]. The mechanisms of constric-
tion in postoperative patients, in patients with collagen vascular disease, and those
with rare hereditary mulbrey nanism, remain unresolved [63, 64].
© The Author(s), under exclusive license to Springer Nature Singapore Pte
Ltd. 2023
U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive
Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_6
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The heart with a normal pericardium can accommodate physiological changes in
cardiac volume during respiration. For example, during inspiration there is a
decrease in intrathoracic pressure which is reected in cardiac chambers.
In constrictive pericarditis, the pericardium is diseased, inelastic and scarred;
hence total cardiac volume cannot change. The rigid, non-pliable pericardial shell
encasing the heart sharply accentuates ventricular pressure-volume relationship
through several mechanisms [27, 28].
As highlighted by Hurrell and colleagues, the tight ventricular interaction in conjunction with insulation of cardiac chambers from variations in intrathoracic pressure during respiratory cycle denes the two key mechanisms underlying the
pathophysiology of chronic constrictive pericarditis, resulting in dissociation of
intrathoracic and intracardiac pressures, and exaggerated ventricular interdependence [27, 28].
6 Pathophysiology ofChronic Constrictive Pericarditis
6.1 Dissociation ofIntrapericardial
andIntrathoracic Pressures
In normal conditions during the respiratory cycle, the difference between left ventricular diastolic pressure and pulmonary capillary wedge pressure remains constant. In constrictive pericarditis, the reduction in intrathoracic pressure during
inspiration is transmitted to the extracardiac pulmonary veins, but not to the left
atrium and left ventricle encased by pericardium, resulting in reduced left ventricular diastolic lling during inspiration.
As a result, there is underlling of left ventricle and reciprocally increased right
ventricular lling. Conversely, there is decrease in right ventricle lling and increase
in left ventricle lling during expiration. This phenomenon of enhanced ventricular
interaction is typical of constrictive pericarditis, and is absent in restrictive
cardiomyopathy.
6.2 Exaggerated Ventricular Interdependence
The second physiologic hallmark of constrictive pericarditis results from marked
ventricular interdependence. Since the total cardiac volume is xed by the nonpliable pericardium, the total volume entering the constricting heart does not vary
signicantly during the respiratory cycle, and there is interdependence of volume
between right and left ventricles. During inspiration, with decrease in left ventricular diastolic volume and lling, there is compensatory increase in right ventricular
lling [61]. Since the inferior caval vein is exposed to variations in intrathoracic
pressure, distended right atrium receives most of the ow from the inferior caval
vein during inspiration, accompanied by increase in inspiratory intraabdominal
6.2 Exaggerated Ventricular Interdependence
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pressure. The ventricular septum is not directly affected by the pericardium and is
free to bulge into the right ventricle, causing a reduction in ow velocity in the
venae cavae and decreased trans-tricuspid ow velocity [56]. In restrictive cardiomyopathy, the variation in respiratory intrathoracic pressures is transmitted normally to all the cardiac chambers due to normal pericardial compliance.
The third major effect of constrictive pericarditis on cardiac haemodynamics is
elevated end-diastolic pressures of all cardiac chambers secondary to impaired diastolic lling [17, 18, 45–49, 57–60]. There is limited cardiac lling in cardiac tamponade from the beginning of diastole, while lling is not restricted in early diastole
in constriction. Contracted, stiff and non-compliant pericardium prevent the normal
distension of ventricles upon lling.
Normally, almost three-fourth of ventricular lling happens during rapid lling
phase of diastole, while atrial contraction contributes to 10–20% of ventricular lling. In constrictive pericarditis, because of elevated atrial pressures, rst 25–30% of
diastole contributes to 70–80% of diastolic lling [36, 54, 55]. Filling rapidly
declines by mid-diastole, and is severely limited in late diastole. This sudden rise in
diastolic pressure presents as “dip and plateau” sign or “square root” sign during
cardiac catheterization [54, 55]. As the distended ventricles reach against non-pliable scarred pericardium, there is interruption in uninhibited diastolic lling,
appearing as abrupt dip on tracing. During relaxation, the ventricles spring back and
are limited by thickened and rigid brotic pericardial sac, resulting in a gentle elevation in diastolic pressure that appears as a plateau tracing. Similarly, tracing of right
atrial pressure reveals a deep Y descent, correlating to the nadir of “square-root”
sign. Under normal circumstances, right atrial pressure drops by 3–7mmHg during
inspiration, causing acceleration of venous return into the heart from neck veins.
The right atrium is prevented by the pericardial constriction to accept inspiratory
accelerated venous return from neck veins resulting in distention of neck veins.
Prominent distened neck veins during inspiration is known as Kussmaul’s sign
(Figs.6.1, 6.2, 6.3, 6.4, 6.5, 6.6, and 6.7) [54, 55].
Tachycardia would adversely affect ventricular lling during diastole in a normal
patient. In patients with constrictive pericarditis, where nearly all ventricular lling
occurs by mid-diastole, tachycardia becomes an important means of maintaining
cardiac output.
During cardiac catheterisation, the diagnosis of constrictive pericarditis is made
based on the presence of various pathophysiological ndings as enumerated under:
(i) All cardiac chambers having equal end-diastolic pressure: The end-diastolic
pressures of left and right ventricles are typically within 5mmHg. But this
criterion has 38% specicity and 60% sensitivity for chronic constrictive
pericarditis;
(ii) Elevated mean atrial pressure: Presence of mean atrial pressure of more than
10mmHg suggests either constrictive pericarditis or cardiac tamponade;
(iii) Tracing of left ventricular pressure shows square root sign;
(iv) Tracing of right-atrial pressure shows prominent “Y” descent;
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Fig. 6.1 Pressure tracing during cardiac catheterization in a patient with chronic constrictive pericarditis showing typical elevation and equalization of right and left ventricular end-diastolic pressure as well as the ‘dip and plateau’ or the ‘square root’ sign
6 Pathophysiology ofChronic Constrictive Pericarditis
Fig. 6.2 Pressure tracing during cardiac catheterization in a patient with chronic constrictive pericarditis showing rapid x and y descents, resembling a “w” pattern. Although this nding is classical of chronic constrictive pericarditis, it can also be seen in restrictive cardiomyopathy
(v) Raised end-diastolic pressure in right ventricle: Typically, there is raised end-
diastolic pressure in right ventricle and typically more than one-third of sys-
tolic pressure in right ventricle. For constrictive pericarditis, this criterion has
93% sensitivity and 57% specicity;
(vi) Ejection fraction of left ventricle: Ideally in chronic constrictive pericarditis
the ejection fraction of left ventricle is 40% or more (Figs.6.1, 6.2, 6.3, 6.4,
6.5, 6.6, and 6.7) [1].
Although the above haemodynamic ndings in isolation may not be diagnostic of
constrictive pericarditis, Vaitkus and Kussmaul demonstrated the predictive accuracy of three haemodynamic criteria.To diagnose constrictive pericarditis, the
ab
6.2 Exaggerated Ventricular Interdependence
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Fig. 6.3 (a) Hemodynamic tracing from a patient with constrictive pericarditis showing elevated
mean right atrial (RA) pressure with rapid x and y descent, resembling a ‘w’ pattern. The y descent
of right atrial pressure tracing corresponds to the rapid lling phase of right ventricular pressure
tracing. (b) Right ventricular (RV) pressure tracing of the same patient with constrictive pericarditis which demonstrates the typical dip and plateau pattern (classical square root sign)
sensitivity of criterions like systolic pressure of right ventricle less than 50mmHg,
ratio of end-diastolic pressure of right ventricle to systolic pressure of right ventricle
more than 1.3 and a difference between end-diastolic pressures of left and right
ventricles of less than 5mmHg is 85%, 75%, and 70% respectively. When all the
three criterions are present, the likelihood of diagnosis of constrictive pericarditis is
more than 90%. [28, 65]
The diagnosis of restrictive cardiomyopathy is made based on following criterions: (i) a normal or small sized heart, (ii) raised jugular venous pressure with prominent X and Y descents, (iii) hepatic congestion, (iv) pulmonary congestion, (v)
absence of ventricular dilation or hypertrophy, and (vi) decreased systolic ventricular function [1–5, 28, 32, 35, 39, 40, 57–60, 72].
But, none of these criterions are pathognomonic for diagnosing restrictive cardiomyopathy, although other non-specic ndings which may provide clues to
either diagnoses include thickened pericardium on echocardiography in constrictive
pericarditis, depressed ejection fraction in restrictive cardiomyopathy, decreased
early diastolic lling in restrictive cardiomyopathy, convergence in end-diastolic
pressure of ventricles in constrictive pericarditis, divergence in end-diastolic pressure of ventricles in restrictive cardiomyopathy, and presence of normal histopathology in chronic constrictive pericarditis.
Hurrell and colleagues studied the respiratory variation during rapid diastolic
lling of the gradient between pulmonary capillary wedge pressure and enddiastolic pressure in left ventricle [5–8, 28, 59, 60, 65]. They assessed the dissociation of intracardiac and intrathoracic pressure in patients with chronic constrictive
pericarditis. Presence of a difference of 5mmHg in the gradient between inspiratory
and expiratory values had sensitivity of 93% and specicity of 81% for diagnosing
constrictive pericarditis [28, 60].
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a
b
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6 Pathophysiology ofChronic Constrictive Pericarditis
Fig. 6.4 (a) Hemodynamic tracing from a patient with chronic constrictive pericarditis showing
the phenomenon of ventricular interdependence of the right ventricular (RV) and left ventricular
(LV) pressures. In constrictive pericarditis, the total ventricular volume is xed by the noncompliant pericardium. With inspiration, the right ventricular (RV) systolic pressure increases with a
corresponding decrease left ventricular (LV) systolic pressure. Exactly reverse happens during
expiration. (b) Ventricular pressure tracings from a patient with restrictive cardiomyopathy. The
right ventricular (RV) and left ventricular (LV) pressure move concordantly with respiration
Systolic pressure of left and right ventricles were compared during respiration to
assess the increase in ventricular interdependence. Although during inspiration
there is expected concordant increase in systolic pressure of left ventricle and right
ventricle, discordant pressures during inspiration in patients is seen in constrictive
pericarditis. This particular nding had a sensitivity of 100% and specicity of 95%
for diagnosing constrictive pericarditis [27, 61].
ab
6.2 Exaggerated Ventricular Interdependence
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Fig. 6.5 (a) High-delity simultaneous pressure tracings of both right and left ventricles during
inspiration and expiration in a patient with constrictive pericarditis showing left and right ventricular
interdependence. During inspiration, LV systolic pressure decreases while RV systolic pressure
increases, and reverse happens during expiration. This respirophasic ventricular interdependence is
absent in restrictive cardiomyopathy. (b) Showing dissociation of intracavitary and intrathoracic
pressures in constrictive pericarditis. In constrictive pericarditis, there is greater fall in pulmonary
capillary wedge pressure (PCWP) than left ventricular (LV) diastolic pressure during inspiration.
Conversely, during expiration, positive intrathoracic pressure leads to an increase in ventricular lling
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Fig. 6.6 Dissociation of intrapericardial and intrathoracic pressures in constrictive pericarditis. In
patients with constrictive pericarditis, the reduction of intrathoracic pressure during inspiration is
transmitted to the extracardiac pulmonary veins, but not to the left atrium and left ventricle resulting in underlling of the left ventricle and reciprocally increased right ventricular lling.
Conversely, there is decreased right ventricular lling and increased left ventricular lling during
expiration. These respiratory effects are manifested by changes in the pressure gradient between
the pulmonary capillary wedge pressure and ventricular early diastolic pressure (arrows)
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