Constrictive Pericarditis vs. Restrictive Physiology

RDCS Adult Echocardiography AE

Track your progress as you read

Finished sections get a check mark.

1 Introduction & Exam Overview

The RDCS AE Exam, SPI Requirement & Logistics Content Outline, Domain Weights & How to Study

2 Cardiac Anatomy

Chambers, Walls, Myocardial Layers & the 17-Segment Model Cardiac Valves & Subvalvular Apparatus Great Vessels, Pericardium, Coronary & Venous Anatomy

3 Cardiac Physiology & Hemodynamics

Cardiac Cycle, Phases & Pressure-Volume Relationships Normal Systolic & Diastolic Function Hemodynamic Principles & Response to Stress

4 Echo Modalities, Instrumentation & Contrast

2D (B-Mode) and M-Mode Imaging Spectral, Color, and Tissue Doppler Modalities Image Optimization, Artifacts, and Contrast Echocardiography

5 Standard Views, Windows & Protocol

Parasternal Long- & Short-Axis Views Apical Views Subcostal & Suprasternal-Notch Views Exam Protocol, Patient Positioning & Provocative Maneuvers

6 Quantification & Doppler Hemodynamic Calculations

Chamber Quantification: LV, LA, RA, and RV Size, Mass, and Volumes Systolic Function: Ejection Fraction Methods, Fractional Shortening & Strain Diastolic Function Grading (ASE/EACVI 2016) Core Doppler Math: Modified Bernoulli, VTI, Stroke Volume & the Continuity Equation Advanced Hemodynamics: PISA/EROA, Pressure Half-Time, dP/dt, Qp/Qs & RVSP

7 Aortic & Mitral Valve Disease

Aortic Stenosis Aortic Regurgitation Mitral Stenosis Mitral Regurgitation

8 Right-Sided, Prosthetic & Infective Valve Disease

Tricuspid & Pulmonic Valve Disease and Pulmonary Hypertension Assessment Infective Endocarditis and Vegetations Prosthetic Valves and Postoperative Evaluation

9 Ischemic Disease & Cardiomyopathies

Coronary Anatomy, Ischemic Heart Disease & Wall-Motion Abnormalities Stress Echocardiography & Myocardial Viability Mechanical Complications of Myocardial Infarction Dilated & Restrictive Cardiomyopathy Hypertrophic Cardiomyopathy, SAM & LVOT Obstruction

10 Pericardial Disease, Masses & Aorta

Pericardial Effusion & Cardiac Tamponade Constrictive Pericarditis vs. Restrictive Physiology Cardiac Masses, Tumors & Thrombi Aortic Disease: Aneurysm, Dissection & Atheroma

11 Congenital Heart Disease & Shunts

Septal Defects & Shunt Quantification Common Adult Congenital Lesions

12 Clinical Care & Safety

Patient Care, Clinical-Data Integration & Exam Protocols Bioeffects, ALARA, Infection Control & Ergonomics

Constrictive Pericarditis vs. Restrictive Physiology

Key Takeaways Explain This Topic AI

Septal bounce and respirophasic septal shift, caused by ventricular interdependence within a rigid pericardium, are hallmark constrictive-pericarditis signs absent in restrictive cardiomyopathy.

Annulus reversus — medial (septal) e′ velocity exceeding lateral e′ velocity — occurs in constriction because the lateral wall is tethered by the diseased pericardium.

Medial e′ velocity is typically preserved or increased (≥8 cm/s) in constrictive pericarditis but reduced (<8 cm/s) in restrictive cardiomyopathy.

Hepatic vein diastolic flow reversal predominates in expiration in constrictive pericarditis and in inspiration in restrictive cardiomyopathy.

Mitral inflow respiratory variation exceeds 25% in constriction but is typically under 10% in restrictive cardiomyopathy, whose filling pattern is already maximally restrictive.

Last updated: July 2026

Constrictive Pericarditis: Pathophysiology

Constrictive pericarditis results from a thickened, fibrotic, and often calcified pericardium that loses its normal compliance, encasing the heart in a rigid shell. Total cardiac volume becomes fixed, so early diastolic filling is rapid — driven by the atrioventricular pressure gradient — but abruptly halts once the fixed pericardial volume is reached, producing the "dip-and-plateau" or "square-root sign" on invasive pressure tracings. Because the rigid pericardium isolates the heart from normal respiratory pressure swings, intrathoracic and intracardiac pressures become dissociated, producing exaggerated ventricular interdependence and respirophasic septal motion — features that are not present in restrictive cardiomyopathy, where the myocardium itself, not the pericardium, is the diseased structure.

Key Echocardiographic Signs of Constriction

Septal bounce (septal shudder) : an abrupt, early-diastolic posterior "bounce" of the interventricular septum, best appreciated on M-mode through the septum, reflecting the sudden cessation of ventricular filling.

Respirophasic septal shift : with inspiration the septum shifts leftward (toward the LV); with expiration it shifts rightward (toward the RV) — the direct 2D correlate of dissociated intrathoracic and intracardiac pressures.

Annulus reversus : medial (septal) mitral annular e′ velocity exceeds lateral annular e′ velocity — the reverse of the normal pattern, in which lateral e′ exceeds medial e′ — because the lateral wall is tethered by the diseased pericardium while the septum moves relatively freely.

Preserved or increased medial e′ : medial e′ is typically ≥8 cm/s, sometimes supranormal, despite a restrictive-appearing transmitral inflow pattern — a key differentiator from restrictive cardiomyopathy, where tissue Doppler velocities are reduced.

Hepatic vein flow reversal in expiration : diastolic flow reversal is exaggerated and predominates during expiration in constriction, mirroring the respirophasic septal shift.

Mitral inflow respiratory variation >25% , the same threshold used for tamponade, reflecting the same exaggerated ventricular interdependence.

IVC plethora , common to constriction, tamponade, and restrictive physiology alike, reflecting elevated right-sided filling pressure.

Restrictive Cardiomyopathy: The Key Differential

Restrictive cardiomyopathy results from infiltrative or fibrotic myocardial disease — cardiac amyloidosis, sarcoidosis, hemochromatosis, endomyocardial fibrosis — producing a stiff, non-compliant myocardium. Filling is restrictive (high E/A ratio, short deceleration time) similarly to constriction, but because the disease resides in the myocardium itself, not an external constraining shell, septal bounce and respirophasic septal shift are absent, and tissue Doppler velocities are reduced rather than preserved.

Differentiating Constriction from Restriction

Feature Constrictive Pericarditis Restrictive Cardiomyopathy
Septal bounce Present Absent
Respirophasic septal shift Present Absent
Medial e′ velocity Preserved/increased (≥8 cm/s) Reduced (<8 cm/s, often <5 cm/s)
Annulus reversus (medial e′ > lateral e′) Present Absent
Hepatic vein diastolic flow reversal Predominates in expiration Predominates in inspiration
Mitral inflow respiratory variation >25% Typically <10%
Pericardium Thickened ± calcified Normal
BNP Normal or mildly elevated Often markedly elevated

Additional adjunctive clues sharpen the distinction further. Longitudinal strain is relatively preserved in constriction, since the myocardium is intrinsically normal, but reduced in restrictive cardiomyopathy — sometimes with a characteristic "apical sparing" pattern in cardiac amyloidosis. When echo findings remain equivocal, cardiac MRI (pericardial thickening, late gadolinium enhancement, real-time cine imaging of septal bounce) or cardiac catheterization with simultaneous LV/RV pressure tracings (concordant versus discordant respiratory pressure changes) can clarify the diagnosis.

Etiology and Additional Diagnostic Clues

Constrictive pericarditis most often follows viral/idiopathic pericarditis, cardiac surgery, mediastinal radiation therapy, or, in endemic regions, tuberculosis; any process causing chronic pericardial inflammation can lead to fibrosis and calcification over months to years. Because calcification is common, a heavily calcified pericardium on 2D imaging — sometimes better appreciated on chest CT — should raise suspicion even before Doppler criteria are formally assessed.

At cardiac catheterization, simultaneous LV and RV pressure tracings show concordant respiratory pressure changes (both ventricular systolic pressures rise or fall together with respiration) in restrictive cardiomyopathy, versus discordant changes (LV and RV systolic pressures move in opposite directions with respiration) in constriction — the invasive correlate of the septal shift seen on echo. Some sources describe the preserved-or-increased medial e′ finding in constriction as "annulus paradoxus," emphasizing that tissue Doppler behaves opposite to what the restrictive-looking mitral inflow pattern would predict.

Finally, remember that constriction and restriction sit on a spectrum with effusive-constrictive pericarditis (Section 10.1), in which a coexisting effusion with tamponade physiology is layered on top of an underlying thickened, constrictive pericardium; the diagnosis is confirmed when RA pressure fails to normalize after pericardiocentesis.

Because management differs fundamentally — pericardiectomy is potentially curative for constriction, while restrictive cardiomyopathy is managed medically and may progress to transplantation — correctly distinguishing the two is both a high-yield exam topic and a decision with major treatment implications. The sonographer's structured evaluation of septal motion, tissue Doppler, and hepatic vein flow is often the first data set that points the clinical team toward the correct diagnosis.

A practical bedside sequence reinforces the pattern: start with M-mode through the septum to look for the bounce, add 2D imaging across the respiratory cycle to confirm the septal shift, then move to tissue Doppler at the medial and lateral mitral annulus to check for annulus reversus, and finish with hepatic vein pulsed-wave Doppler timed to respiration. Running through all four in sequence, rather than relying on any single sign in isolation, is what gives the exam-day and real-world diagnosis its accuracy, since no individual finding is perfectly sensitive or specific on its own.