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Haemodynamics of constrictive pericarditis

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The hemodynamics of constrictive pericarditis (CP) are defined by a rigid, noncompliant pericardium that encases the heart, leading to a “fixed” total cardiac volume. This pathological state results in two primary hemodynamic hallmarks: the dissociation of intrathoracic and intracardiac pressures and exaggerated ventricular interdependence.


1. Core Pathophysiological Hallmarks

The rigid pericardial shell insulates the heart from the normal pressure fluctuations of the respiratory cycle.


2. Invasive Hemodynamic Findings

Cardiac catheterization remains a definitive method for identifying the specific “constrictive” profile.

FindingDescriptionMechanism
Square Root SignA rapid early diastolic “dip” followed by a flat “plateau.”Fast early filling that halts abruptly when the rigid pericardium is reached.
Equalization of PressuresDiastolic pressures in all four chambers equalize (within 5 mmHg).The rigid shell dictates a common filling pressure for the entire heart during diastole.
Prominent Y-DescentA sharp, deep drop in atrial/venous pressure at the start of diastole.Reflects the rapid, unimpeded early filling of the ventricles before the pericardial limit is hit.
Kussmaul’s SignA paradoxical rise (or lack of fall) in jugular venous pressure (JVP) during inspiration.The RV cannot accommodate the inspiratory increase in venous return due to the noncompliant shell.

3. Respirophasic Dynamics: The Key Differentiator

The most critical diagnostic finding in the cath lab is ventricular discordance, which helps distinguish CP from restrictive cardiomyopathy (RCM).


4. Non-Invasive Correlates

Modern imaging translates these hemodynamics into visual markers:

References

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