Chapter 15 — Pericardial Disease and Cardiac Tamponade

📚 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.