CardiologyTier 2Disease (DEADMAN)

Pericardial disease - pericardial effusion and tamponade

Description

Pericardium: fibrous + serous, normally 15-50 mL serous fluid
Effusion = accumulation of fluid in the pericardial space
Tamponade = effusion raising intrapericardial pressure to the point of impaired diastolic filling
- A haemodynamic diagnosis, not a size on echo

Rate matters more than volume

Acute (trauma, dissection, post-procedural): 100-200 mL can tamponade - steep pericardial pressure-volume curve
Chronic (malignancy, hypothyroidism, uraemia): >1-2 L tolerated - pericardium stretches
-> A huge chronic effusion may be asymptomatic; a small acute one may kill

Size (echo, end-diastolic separation)


Trivial	<5 mm (systolic only)
Small	<10 mm
Moderate	10-20 mm
Large	>20 mm

Variants

Effusive-constrictive - effusion + visceral constriction; RA pressure stays elevated after drainage
Loculated / regional - post-surgical, can tamponade one chamber only (TTE may miss; TOE needed)
Low-pressure tamponade - hypovolaemic patient, tamponade physiology at low intrapericardial pressure

Epidemiology

Effusion found in ~3-9% of unselected echos
Tamponade incidence ~2/10,000
In the developed world: idiopathic/viral and iatrogenic dominate
Malignancy = commonest cause of large symptomatic effusion presenting de novo
Developing world and Indigenous Australians: TB a leading cause

Aetiopathogenesis

Causes

Idiopathic / viral (~50% in developed settings) - coxsackie, echovirus, adenovirus, EBV, influenza, HIV, SARS-CoV-2
Malignant - lung, breast, lymphoma, melanoma, mesothelioma; direct invasion or lymphatic obstruction
Iatrogenic / traumatic - PCI or coronary perforation, pacemaker lead, ablation, pericardiocentesis, cardiac surgery, CPR, chest trauma
Aortic dissection with rupture into pericardium (type A - immediate surgery, do NOT drain)
Post-MI - free wall rupture (day 3-7), or Dressler (weeks)
Infective - TB (commonest worldwide), purulent (staph, strep, pneumococcus)
Inflammatory / autoimmune - SLE, RA, scleroderma, vasculitis, sarcoid, familial Mediterranean fever
Metabolic - uraemia, hypothyroidism (classic large silent effusion), ovarian hyperstimulation
Drugs - hydralazine, procainamide, isoniazid, minoxidil, immune checkpoint inhibitors
Radiation - mediastinal; may evolve to constriction

Mechanism of tamponade

inc intrapericardial pressure -> equalisation of diastolic pressures across all four chambers
-> dec transmural filling pressure -> dec preload -> dec stroke volume
Compensation: tachycardia + inc SVR (maintain BP until decompensation, then precipitous collapse)
Fixed total cardiac volume -> enhanced ventricular interdependence
- Inspiration -> inc RV filling -> septum bows left -> dec LV filling -> dec LV SV -> pulsus paradoxus
Pulsus paradoxus is an exaggeration of a normal phenomenon, not a reversal

Diagnosis

Clinical

Beck's triad: hypotension + distended neck veins + muffled heart sounds
- Complete triad in a minority; sensitive only in acute tamponade
Tachycardia, tachypnoea, dyspnoea, oliguria
Pulsus paradoxus - inspiratory fall in SBP >10 mmHg
- Absent in: coexisting ASD, severe AR, elevated LVEDP, regional/loculated tamponade, severe hypotension
- Present without tamponade in: severe asthma/COPD, massive PE, obesity, constriction (~1/3)
JVP: elevated with prominent x descent, absent y descent (no early diastolic filling at all)
- Kussmaul sign is absent in tamponade - it belongs to constriction
Ewart sign - dullness/bronchial breathing below left scapula (large effusion)

ECG

Low voltage, sinus tachycardia
Electrical alternans - beat-to-beat QRS amplitude variation from the heart swinging in fluid
- Classic, highly specific, insensitive
PR depression / widespread saddle ST elevation if pericarditic

CXR

Globular "water-bottle" heart - needs >200 mL
Clear lung fields with a big heart -> think effusion

Echo - the diagnostic test

Sign	Detail
RA collapse in late diastole/systole	Earliest; >1/3 of cardiac cycle = specific
RV diastolic collapse	More specific, less sensitive
Any chamber collapse	Sens ~90%, spec ~65%
Respiratory flow variation	Tricuspid inflow inc >40%, mitral inflow dec >25% on inspiration ("echo pulsus")
Septal bounce / leftward shift on inspiration	Interdependence
IVC plethora	Dilated IVC, <50% inspiratory collapse
Swinging heart	Large effusion

LA collapse is the most specific single sign but uncommon
Tamponade is a clinical diagnosis supported by echo - treat the patient, not the images

Cardiac catheterisation (if uncertain)

Equalisation of diastolic pressures: RA = RVEDP = PADP = PCWP (within 5 mmHg)
Blunted/absent y descent
Drainage -> immediate fall in RA pressure and rise in CO
- If RA pressure stays high -> effusive-constrictive

Fluid analysis (when drained)

MCS + AFB + TB PCR, cytology, protein/LDH, glucose, haematocrit, adenosine deaminase (TB)
Cytology sensitivity for malignancy ~70-90%; a negative result does not exclude

Management

A. Tamponade - emergency

Drainage is the only definitive treatment
Holding measures while arranging it:
- IV fluid bolus if hypovolaemic (modest benefit; harmful if filling pressures already very high)
- Avoid vasodilators and diuretics
- Avoid positive pressure ventilation and intubation if at all possible - dec venous return -> arrest
  - If unavoidable, drain first or have the needle ready
Echo-guided pericardiocentesis - subxiphoid or apical, leave a drain until output <25-50 mL/day
Surgical drainage / pericardial window preferred if:
- Purulent, loculated, posteriorly located, traumatic/haemorrhagic, or recurrent malignant effusion
*Do NOT drain: type A aortic dissection or free wall rupture* - relieves tamponade, restores BP, exsanguinates
- -> straight to theatre

B. Effusion without tamponade - treat the cause

Idiopathic/viral - NSAID + colchicine; drainage only if large or diagnostic doubt
- Colchicine halves recurrence
Purulent - urgent drainage + IV antibiotics +/- intrapericardial fibrinolysis
TB - standard 4-drug regimen + corticosteroid in selected (reduces constriction and reaccumulation)
Uraemic - intensify dialysis
Hypothyroid - thyroxine; resolves slowly, rarely needs drainage
Malignant - drainage +/- prolonged catheter, pericardial window, or sclerosis; systemic therapy for the tumour
Autoimmune - treat underlying disease; steroids/IL-1 blockade (anakinra, rilonacept) for recurrent pericarditis

Follow-up

Repeat echo after drainage and before discharge
Idiopathic moderate-large effusion: echo at 1, 3, 6, 12 months

Associations

Acute and recurrent pericarditis - effusion in ~60%
Constrictive pericarditis - especially after TB, radiation, purulent, cardiac surgery
Hypothyroidism - large, slow, silent
Malignancy - lung and breast account for most malignant effusions
Post-cardiac injury syndromes - Dressler, post-pericardiotomy, post-ablation
Connective tissue disease - SLE (may be the presenting feature), RA, systemic sclerosis
Chylopericardium - thoracic duct injury, lymphangioleiomyomatosis
Immune checkpoint inhibitor myocarditis/pericarditis

Natural history & complications

Idiopathic small effusion: usually resolves, benign
Large idiopathic chronic effusion (>3 months): ~30% progress to tamponade unpredictably - consider elective drainage
Malignant effusion: reaccumulates in ~50% after simple drainage; median survival weeks to months
- Presence of malignant effusion is a poor prognostic marker regardless of drainage

Complications

Tamponade and PEA arrest
Effusive-constrictive and constrictive pericarditis
Pericardiocentesis: RV puncture, coronary/hepatic laceration, arrhythmia, pneumothorax, post-decompression pulmonary oedema / acute RV dilatation (drain no more than ~1 L at once)
Recurrence

Distinguishing tamponade from constriction

	Tamponade	Constriction
JVP y descent	Absent	Prominent (steep)
Kussmaul sign	Absent	Present
Pulsus paradoxus	Present	~1/3
Pericardial knock	No	Yes
Filling	Impeded throughout diastole	Impeded in mid-late diastole

6 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.

Get premium access