Constrictive pericarditis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

A scarred or inflamed pericardium dissociates intrathoracic from intracardiac pressure and exaggerates ventricular interdependence. The phenotype resembles restrictive cardiomyopathy but has a different—and potentially surgical—solution.

Diagnosis is physiological and multimodal. Echo is first-line; CT/CMR clarifies anatomy and inflammation, while simultaneous left/right catheterisation resolves difficult cases.

Treatment depends on reversibility. Active inflammatory constriction earns a monitored medical trial; fixed chronic symptomatic disease should reach an experienced pericardiectomy team early.

Key points

Constrictive pericarditis is impaired diastolic filling from a non-compliant pericardium and is a potentially curable cause of predominantly right-sided HF.
Clues are raised JVP, prominent y descent, Kussmaul sign, pericardial knock, ascites and oedema with relatively clear lungs.
Echo looks for ventricular interdependence: septal bounce, respiratory mitral/tricuspid inflow variation and expiratory hepatic-vein diastolic reversal.
Medial mitral e-prime is often preserved or increased and may exceed lateral e-prime ('annulus reversus'), unlike myocardial restriction.
CT defines calcification and thickness; CMR identifies inflammation—but normal thickness does not exclude physiological constriction.
Inflammatory transient constriction may resolve with cause-specific/anti-inflammatory therapy and serial imaging.
Complete pericardiectomy is definitive for persistent symptomatic fixed constriction; refer before cachexia, cirrhosis or severe end-organ dysfunction.
Diuretics relieve congestion but excessive preload reduction can lower output and should not postpone surgical assessment.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Previous cardiac surgery or haemopericardium

Surgical injury, postoperative inflammation or blood within the pericardial space can heal with dense adhesion and fibrosis. Symptoms may emerge months or years after the inciting event.

Recurrent or persistent pericardial inflammation

Repeated inflammatory episodes can organise into a stiff fibrous envelope. When active inflammation remains, some constrictive physiology may be transient rather than permanently scarred.

Tuberculous or bacterial pericarditis

Granulomatous or purulent infection can produce intense inflammation, exudate and subsequent scarring. Identifying infection matters because immunosuppression without cause-specific treatment may be harmful.

Chest radiotherapy

Radiation can fibrose the pericardium, myocardium, valves and coronary vessels. Resulting constriction may therefore coexist with restrictive myocardial or other structural disease.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pericardium stiffens
Pericardial inflammation or injury can produce oedema, adhesion and, in chronic disease, fibrosis or calcification, creating a non-compliant envelope. Physiologically important constriction can occur despite normal pericardial thickness.
2
Diastolic expansion stops abruptly
Ventricles fill rapidly in early diastole until they meet the rigid pericardial limit. Filling then halts, producing raised diastolic pressures and sometimes a pericardial knock.
3
Thoracic pressure is not transmitted normally
During inspiration, intrathoracic pressure falls but the encased chambers do not experience the change fully. Systemic venous return rises against a right ventricle unable to expand.
4
Ventricles become interdependent
Because total cardiac volume is constrained, increased filling of one ventricle shifts the septum and reduces filling of the other. This can create marked respiratory Doppler variation.
5
Venous pressure rises and output falls
Restricted filling produces systemic venous congestion, ascites and oedema, often with relatively clear lungs. Advanced disease limits stroke volume and injures renal and hepatic organs.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Systemic venous congestion

Raised JVP, hepatomegaly, ascites, peripheral oedema, pleural effusions and cachexia may dominate over pulmonary oedema.

Kussmaul sign

JVP fails to fall or rises on inspiration because the constrained right ventricle cannot accept increased venous return.

Pericardial knock

An early diastolic sound occurs earlier than an S3 as rapid filling stops abruptly against the rigid pericardium.

Risk history

Prior cardiac surgery, recurrent pericarditis, chest radiotherapy, TB, bacterial pericarditis and haemopericardium increase suspicion.

Advanced diseaseRed flag

Hypotension, hyponatraemia, renal dysfunction, jaundice/cardiac cirrhosis, severe hypoalbuminaemia or cachexia signals high operative risk and urgent referral.

Effusive-constrictive diseaseRed flag

Persistently elevated right-sided pressure after pericardial drainage suggests visceral-pericardial constriction and needs expert haemodynamic review.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Comprehensive Doppler TTEFirst step
Why
Demonstrate interdependence and distinguish constriction from restriction.
Interpretation and limitations
Seek septal shift, respiratory inflow variation, expiratory hepatic-vein reversal, annulus reversus/paradoxus and IVC plethora as a pattern, not a single sign.
02
ECG, CXR and routine HF laboratory panel
Why
Assess rhythm, calcification/effusions and end-organ impact.
Interpretation and limitations
AF and low voltage are non-specific; visible calcification supports chronicity but its absence does not exclude constriction.
03
CT
Why
Map pericardial thickness, calcification and surgical anatomy.
Interpretation and limitations
Anatomical thickening/calcification supports but does not prove constrictive physiology; normal thickness can occur.
04
CMR
Why
Confirm interdependence and assess pericardial oedema/LGE and myocardial disease.
Interpretation and limitations
Active pericardial inflammation supports a potentially transient phenotype; myocardial infiltration suggests restriction or mixed disease.
05
Simultaneous left- and right-heart catheterisation
Why
Resolve equivocal non-invasive findings and guide surgery.
Interpretation and limitations
Respiratory discordance of LV/RV systolic pressures and dip-and-plateau filling support constriction; simple diastolic pressure equalisation is not specific.
06
Cause-directed testing
Why
Identify TB, malignancy, autoimmune, renal, post-surgical or radiation-related disease.
Interpretation and limitations
Biopsy/fluid is selected when it will change therapy; treatable cause and operative risk should be defined together.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Restrictive cardiomyopathy

Myocardial infiltration or fibrosis also causes high filling pressures, but tissue velocities are usually reduced and respiratory ventricular interaction is less marked. CMR and haemodynamics resolve overlap.

Cardiac tamponade

A pressurised effusion limits filling and can cause hypotension and raised jugular venous pressure. Echo evidence of effusion with chamber collapse differs from chronic constrictive respiratory physiology.

Severe tricuspid regurgitation

Tricuspid regurgitation produces systemic congestion, prominent jugular v waves and systolic hepatic-vein flow reversal. A primary valve lesion without the characteristic constrictive respiratory pattern favours severe tricuspid regurgitation.

Pulmonary hypertension with right-heart failure

Raised pulmonary pressure causes right-ventricular dilatation, dysfunction and congestion. Pulmonary haemodynamics and the absence of a constrictive respiratory interaction help distinguish it from isolated constriction.

Cirrhosis or portal hypertension

Primary liver disease can cause ascites, oedema and hypoalbuminaemia, but usually lacks a markedly raised jugular venous pressure and constrictive cardiac imaging features.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01DiagnosisSuspected constrictive physiologyFirst stepUnexplained right HF/HFpEF with pericardial risk or JVP signs.

1Obtain expert Doppler echo and review prior surgery, radiation, pericarditis, TB and malignancy; assess liver/renal/nutritional status.
2Use CT for thickness/calcification and CMR for inflammation, interdependence and myocardial differential.
3If echo/CMR are discordant or restriction remains plausible, perform simultaneous left/right haemodynamics at an experienced centre.
4Classify as transient inflammatory, chronic fixed, effusive-constrictive or mixed myocardial-pericardial disease before choosing therapy.

02TransientInflammatory constrictionRecent pericarditis with elevated CRP and/or pericardial oedema/LGE, without advanced fixed disease.

1Treat the identified cause and use aspirin/NSAID plus colchicine when appropriate; avoid empirical immunosuppression until infection, especially TB, is excluded.
2Use cautious diuretic for congestion and define a 3-6 month reassessment window with symptoms, CRP and echo/CMR physiology.
3If inflammation and constriction resolve, taper therapy gradually and continue surveillance; if physiology persists or end-organ function declines, stop waiting and refer for surgery.

03FixedPersistent symptomatic constrictionConfirmed chronic physiology with symptoms despite medical management.

1Refer early to a high-volume pericardiectomy team for complete resection assessment; quantify liver, renal, nutritional, coronary and radiation-related risk.
2Use the lowest effective diuretic while awaiting surgery and address AF, pleural effusion, nutrition and the underlying cause.
3Do not defer until irreversible cirrhosis/cachexia; if surgery is prohibitive, provide specialist symptom and advanced-HF care with explicit prognosis.

04Specific causeTB, purulent, malignant or radiation diseaseExposure, systemic signs, fluid/tissue or imaging points to a secondary cause.

1For TB or bacterial disease, obtain microbiology/tissue and start specialist antimicrobial therapy; drainage is required for purulent collections.
2For malignancy, coordinate oncology, cytology/biopsy and recurrence control; for radiation, assess concomitant myocardial, valve and coronary disease.
3Reassess surgical benefit after cause staging because extensive myocardial or malignant disease may alter the risk-benefit balance.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Temporary symptom control of oedema/ascites while defining reversibility or awaiting surgery.

Furosemide

Common oral starting dose 20-40 mg once daily, titrated cautiously to congestion.

Constriction is preload-dependent; overdiuresis can cause low output, hypotension, renal injury and hyponatraemia. It is not definitive treatment.

Time-limited anti-inflammatory component when imaging/markers support transient pericardial inflammation.

Ibuprofen

600 mg orally three times daily for active inflammatory constriction, then taper after clinical and CRP remission; maximum 2400 mg/day.

Do not use for fixed non-inflammatory constriction. Renal, GI, bleeding, HF and pregnancy risks require review.

Adjunct for active pericardial inflammation, not a mechanical cure for scarred constriction; UK use is off-label.

Colchicine

0.5 mg orally once daily at 70 kg or less, or twice daily if over 70 kg; duration is specialist-led according to the inflammatory syndrome.

In mild or moderate renal or hepatic impairment use 0.5 mg once daily; severe impairment is contraindicated. Do not combine with strong CYP3A4/P-gp inhibitors when renal or hepatic function is impaired. Diarrhoea, cytopenia and myopathy can signal toxicity.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Refractory systemic congestion

Persistently high venous pressure causes ascites, peripheral oedema, pleural effusions and severe exercise limitation. Diuretic dependence may increase while excessive preload reduction lowers output.

Congestive hepatopathy and cirrhosis

Longstanding hepatic venous congestion causes cholestatic dysfunction, fibrosis and eventually cardiac cirrhosis. Advanced liver injury raises operative risk and may limit postoperative recovery.

Cardiorenal low-output syndrome

Restricted ventricular filling reduces forward flow while venous pressure impedes renal drainage. Progressive renal dysfunction, hyponatraemia, hypotension and treatment intolerance can follow.

Malnutrition and cachexia

Gut oedema, hepatic dysfunction and chronic inflammatory illness impair appetite and nutrient absorption. Hypoalbuminaemia, muscle loss and frailty signal advanced disease and poorer surgical resilience.

Atrial arrhythmia

Chronic atrial pressure and enlargement can promote atrial fibrillation or flutter. Loss of coordinated filling may further reduce cardiac output and increase thromboembolic risk.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Trend weight, oedema/ascites, JVP, BP, exercise tolerance and diuretic requirement.
Check renal function, sodium, potassium, LFT, albumin and INR to detect end-organ deterioration and operative risk.
In transient disease, follow CRP and repeat Doppler echo/CMR within the defined 3-6 month window.
Monitor AF/rate and pleural effusions; rhythm loss may worsen filling markedly.
During surgical assessment, document nutrition, frailty, coronary anatomy and concomitant myocardial/valve/radiation disease.
After pericardiectomy, reassess residual filling abnormalities and congestion; improvement may be gradual and incomplete in mixed disease.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Thickness is not physiology

A thick or calcified pericardium can be incidental, and proven constriction can occur with normal thickness.

Annulus reversus

Medial e-prime may exceed lateral e-prime because lateral annular motion is tethered by the pericardium.

BNP can help, not decide

BNP is often lower in pure constriction than myocardial restriction, but renal disease, AF and mixed radiation injury create substantial overlap.

Transient disease earns a clock

A medical trial should have objective inflammation and a defined reassessment date; indefinite delay allows end-organ damage.

Radiation is often mixed

Pericardiectomy may not normalise symptoms when myocardial restriction, coronary and valve disease coexist.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing constriction from calcification alone or excluding it because pericardial thickness is normal.
02
Relying on one echo sign without respiratory physiology and clinical context.
03
Continuing escalating diuretics while delaying potentially curative surgery.
04
Giving immunosuppression for presumed transient constriction before excluding TB/bacterial disease.
05
Assuming all right HF after chest radiotherapy is purely pericardial.