📚 Guideline basis
Klein AL, Abbara S, Agler DA, et al. ASE clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease (JASE 2013;26:965–1012); 2015 ESC guidelines for the diagnosis and management of pericardial diseases; ASE 2025 diastolic function update (constriction section); Mayo Clinic criteria for constrictive pericarditis (Welch TD, et al., Circ Cardiovasc Imaging 2014).
Pathophysiology & Mechanisms
The pericardial pressure–volume relationship
The normal pericardium contains 15–50 mL of serous fluid and is a stiff, minimally compliant sac. Its pressure–volume curve is J-shaped and steep: it accommodates a modest volume with little pressure rise, then rises almost vertically.
Two consequences dominate every clinical decision in this chapter:
- Rate matters more than volume. An acutely accumulating 150–250 mL produces tamponade; a chronically accumulating 1000–2000 mL, which has allowed the pericardium to stretch, may not. Volume alone never grades tamponade.
- Tamponade is a physiological diagnosis, not an imaging one. A large effusion without haemodynamic consequence is an effusion; a small loculated effusion compressing one chamber is tamponade.
Tamponade physiology
Rising intrapericardial pressure equalises the diastolic pressures of all four chambers at the pericardial pressure. Total cardiac volume becomes fixed, and the ventricles compete for a fixed space — exaggerated ventricular interdependence.
During spontaneous inspiration, negative intrathoracic pressure augments right-sided filling; because total volume is fixed, the septum shifts left, LV filling falls, and stroke volume and systemic pressure fall. This is the mechanism of pulsus paradoxus and of the respiratory inflow variation seen on Doppler.
Under positive-pressure ventilation the physiology inverts. Inspiration raises intrathoracic pressure, reduces venous return, and the direction and magnitude of the respiratory variation change. The conventional thresholds — mitral variation ≥ 25%, tricuspid ≥ 40% — were derived in spontaneously breathing patients and are unreliable in the ventilated patient. This is stated once here and repeated in the pitfalls, because it is the commonest reason tamponade is missed in the ICU.
Diagnostic Synthesis
Effusion characterisation
Feature | Assessment |
Size (end-diastole) | Small < 10 mm; moderate 10–20 mm; large > 20 mm |
Distribution | Circumferential vs loculated (post-surgical, post-inflammatory) |
Character | Anechoic (serous) · echodense or stranded (haemorrhagic, purulent, malignant) · fibrinous strands · frank clot |
Mimics | Epicardial fat pad — anterior, hypoechoic, granular, moves with the heart; pleural effusion — extends posterior to the descending thoracic aorta whereas pericardial fluid tracks anterior to it (Chapter 3) |
Tamponade signs, ranked by what they are good for
Sign | Mechanism | Property |
Right atrial systolic collapse | The thinnest-walled chamber at its lowest pressure | Sensitive; becomes specific when it persists for more than one-third of the cardiac cycle |
Right ventricular diastolic collapse | Pericardial pressure exceeds early-diastolic RV pressure | Specific, less sensitive; occurs later |
Plethoric IVC with < 50% collapse | Elevated right atrial pressure | Sensitive; a normal, collapsing IVC argues strongly against tamponade in a spontaneously breathing patient |
Mitral inflow respiratory variation ≥ 25% | Ventricular interdependence | Supportive; unreliable under positive-pressure ventilation |
Tricuspid inflow respiratory variation ≥ 40% | Same | Same caveat |
Hepatic vein expiratory diastolic flow reversal | Impaired diastolic filling | Supportive |
Swinging heart | Large effusion with free cardiac motion | Associated with electrical alternans |
Left atrial or left ventricular collapse | Localised pressure | Uncommon; typical of loculated post-surgical collections |
A normal, fully collapsing IVC in a spontaneously breathing patient is the most useful single negative finding. It makes tamponade physiology very unlikely.
Special situations
Situation | Why the standard picture fails |
Post-cardiotomy | Loculated, posterior, frequently clot; any single chamber may be compressed; respiratory variation absent; TTE frequently cannot see it — TEE is required (Chapter 36) |
Positive-pressure ventilation | Respiratory variation thresholds invalid; diagnose on chamber collapse, IVC plethora and the clinical trajectory |
Low-pressure tamponade | In the hypovolaemic patient (haemorrhage, dialysis, dehydration), intracardiac pressures are low, so a modest effusion tamponades at a low intrapericardial pressure with subtle signs. The effusion may only tamponade after diuresis |
Elevated right-sided pressures (pulmonary hypertension, RV hypertrophy) | The stiff, high-pressure RV resists collapse; chamber-collapse signs may be absent despite tamponade |
Trauma | Small volumes tamponade acutely; a concurrent pericardial tear may decompress into the pleura, producing a falsely reassuring pericardial window (Chapter 37) |
Regional tamponade | Compression of a single chamber or a pulmonary vein by a localised collection or haematoma |
Constrictive physiology
Constriction and restriction both produce a small, stiff heart with elevated filling pressures and clinically similar presentations, and separating them determines whether the patient goes to surgery.
Mechanisms
Constriction has two defining features absent in restriction: dissociation of intrathoracic and intracardiac pressures (the rigid pericardium shields the heart from respiratory pressure swings) and enhanced ventricular interdependence.
Findings
Finding | Detail |
Respirophasic ventricular septal shift | Septum moves toward the LV on inspiration and toward the RV on expiration — the single most important sign |
Septal bounce | Early-diastolic abrupt septal motion |
Mitral inflow respiratory variation | > 25% |
Tricuspid inflow respiratory variation | > 40% |
Hepatic vein expiratory diastolic flow reversal | Reversal/forward ratio ≥ 0.8 (ASE 2025) or ≥ 0.79 (Mayo criteria) |
Medial (septal) mitral annular e′ | Preserved or increased — ASE 2025 states it is often > 7 cm/s; the Mayo criteria use ≥ 9 cm/s. Contrast with restriction, where it is typically ≤ 5 cm/s |
Annulus reversus | Septal e′ exceeds lateral e′ — the reverse of normal, from lateral wall tethering by the adherent pericardium |
Strain reversus | Lateral LV and RV free wall peak systolic strain reduced relative to septal |
Pericardial thickening / calcification | Supportive; often better seen on CT — and absent thickening does not exclude constriction |
The Mayo algorithm requires respirophasic septal shift plus either a medial e′ ≥ 9 cm/s or a hepatic vein expiratory diastolic reversal ratio ≥ 0.79, with reported sensitivity around 87% and specificity around 91%.
Constriction versus restriction
Feature | Constriction | Restrictive cardiomyopathy |
Septal e′ | Normal or increased (> 7–9 cm/s) | Reduced (3–5 cm/s) |
Annulus reversus | Present | Absent |
Respirophasic septal shift | Present | Absent |
Mitral inflow respiratory variation | > 25% | Minimal |
Hepatic vein reversal | Expiratory | Inspiratory |
Pericardium | May be thickened/calcified | Normal |
Atrial size | Moderately enlarged | Markedly biatrially enlarged |
Wall thickness | Normal | Often increased (amyloid) |
A normal septal e′ in a patient carrying a heart failure diagnosis should raise suspicion of constriction. This is the single most useful discriminating observation, and it is counter-intuitive because normal tissue Doppler is usually reassuring.
Effusive-constrictive pericarditis — persistent elevation of right atrial pressure after drainage of an effusion — is diagnosed when constrictive physiology emerges once the effusion is removed.
Pericardiocentesis
Step | Detail |
Site selection by ultrasound, not by landmark | Choose the point of maximal fluid depth closest to the skin with no intervening structures — most often apical or left parasternal, not subxiphoid |
Approach | In-plane needle visualisation where possible; measure the depth to fluid before starting |
Confirmation of position | Inject a small volume of agitated saline through the needle or catheter — opacification of the pericardial space confirms position and excludes intracardiac placement |
Drainage | Catheter placement over a guidewire; drain to dryness with serial imaging |
Post-procedure | Repeat imaging to confirm resolution and to look for effusive-constrictive physiology |
Pericardial decompression syndrome | Paradoxical haemodynamic deterioration or pulmonary oedema after drainage; uncommon, described after rapid removal of large volumes; mitigated by staged drainage |
When not to drain: tamponade from type A aortic dissection or from free wall rupture — removing the tamponade removes the tamponade effect that is limiting haemorrhage, and can precipitate exsanguination. These require surgery, not a needle.
ICU-Specific Limitations
Confounder | Effect | Response |
Positive-pressure ventilation | Respiratory variation thresholds invalid; IVC behaviour altered | Diagnose on chamber collapse, IVC plethora, clinical trajectory |
Post-sternotomy | Loculated posterior clot invisible on TTE | Early TEE |
Hypovolaemia | Masks tamponade until volume is restored or removed | Consider low-pressure tamponade; reassess after fluid |
Pulmonary hypertension / RV hypertrophy | Chamber collapse signs absent | Rely on the physiology and the clinical picture |
Poor windows, drains, emphysema | Effusion may be missed entirely | Subcostal; TEE |
Atrial fibrillation | Respiratory variation uninterpretable | Chamber collapse and IVC |
🛑 Critical pitfall: Excluding tamponade because respiratory inflow variation is below threshold in a ventilated patient. The thresholds were derived during spontaneous breathing and do not apply.
🛑 Critical pitfall: Grading tamponade by effusion size. An acute 150 mL haemopericardium can arrest a patient; a chronic litre may be asymptomatic.
🛑 Critical pitfall: Draining a pericardial effusion caused by type A dissection or free wall rupture. The tamponade is limiting the bleeding; this is a surgical problem.
- 💡 Clinical pearl: Right atrial systolic collapse lasting more than one-third of the cardiac cycle converts a sensitive sign into a specific one. Measure it against the ECG rather than eyeballing it.
- 💡 Clinical pearl: In an unexplained low-output state after cardiac surgery, assume loculated tamponade and get a TEE. The negative transthoracic study is not reassurance.
- 💡 Clinical pearl: A normal or high septal e′ in a congested patient is the clue to constriction — and it is the one finding that will otherwise be read as reassuring.
References
- Klein AL, Abbara S, Agler DA, et al. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease. J Am Soc Echocardiogr 2013;26:965–1012.
- Adler Y, Charron P, Imazio M, et al. 2015 ESC guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015;36:2921–64.
- Welch TD, Ling LH, Espinosa RE, et al. Echocardiographic diagnosis of constrictive pericarditis: Mayo Clinic criteria. Circ Cardiovasc Imaging 2014;7:526–34.
- Nagueh SF, Sanborn DY, Oh JK, et al. ASE 2025 diastolic function update. J Am Soc Echocardiogr 2025;38:537–69.