Cardiac Tamponade

Phases of Haemodynamic Change

Phase I

• Initial accumulation of fluid impairs ventricular relaxation, requiring higher filling pressures; ventricular filling pressures remain higher than intrapericardial pressure.

Phase II

• Continued accumulation raises pericardial pressure above chamber filling pressures, reducing cardiac output.

Phase III

• Pericardial and left ventricular diastolic pressures equilibrate, leading to profound falls in stroke volume and systemic perfusion.

Rate of Accumulation and Compliance

• The clinical impact of an effusion depends on how rapidly it develops and the compliance of the pericardium.
• Rapid accumulation (e.g., haemopericardium following trauma or rupture) can provoke tamponade with as little as 150 mL.
• Gradual accumulation (e.g., from malignancy or uraemia) may allow up to 1–2 litres before tamponade occurs due to adaptive stretching.
• Once the elastic limit of the pericardium is reached, even minimal additional fluid can precipitate collapse; conversely, drainage of a small volume produces a large drop in intrapericardial pressure.

Chamber Compression and Venous Return

• Increased pericardial pressure compresses all cardiac chambers when fluid is circumferential, though loculated effusions can produce regional tamponade.
• Venous return is impaired throughout the cardiac cycle, with diastolic filling particularly affected.
• Venous return normally has two peaks—during systole and early diastole. In tamponade, the early diastolic component is diminished, shifting filling predominantly to systole. As severity progresses, overall venous return falls, chambers shrink, and systemic blood pressure drops.

Ventricular Interdependence

• The pericardium restricts expansion, forcing the right and left ventricles to share a fixed volume.
• During inspiration, increased systemic venous return distends the right ventricle, which shifts the interventricular septum leftward. This reduces left ventricular compliance and stroke volume.
• The result is exaggerated inspiratory decline in systolic pressure (pulsus paradoxus).

Equalisation of Pressures

• A hallmark of tamponade is equalisation of diastolic pressures across the right atrium, right ventricle, pulmonary capillary wedge pressure, and left ventricle.
• This pressure uniformity reflects external constraint by the effusion and explains why small variations in chamber compliance can markedly influence clinical presentation.

Compensatory Mechanisms

• Tachycardia is an early adaptive response to maintain cardiac output in the face of reduced stroke volume.
• Systemic venous congestion occurs as blood accumulates in the venous system, further reducing preload to the left heart.
• In advanced stages, hypotension, shock, and cardiac arrest ensue if decompression is not achieved.

Fluid Characteristics

• Pericardial effusions leading to tamponade may be serous, serosanguineous, haemorrhagic, or chylous, depending on the underlying aetiology.
• Adhesions or loculated fluid collections can produce atypical tamponade physiology, with selective chamber compression.

General Incidence

• In the United States, the incidence of cardiac tamponade is estimated at approximately 5 per 10,000 population.
• Among penetrating chest injuries, tamponade occurs in about 2% of cases.
• Hospital-based studies show tamponade may complicate up to 13% of patients admitted with acute pericarditis.
• In those with large, chronic pericardial effusions (>10 mm on echocardiography), incidence ranges between 30% and 44%.

Age and Sex Distribution

• Cardiac tamponade can present at any age, but it is most frequently diagnosed in middle-aged and older adults, reflecting the prevalence of malignancy, renal failure, and chronic inflammatory conditions.
• In paediatric populations, tamponade is more common in boys than girls, with ratios of approximately 7:3.
• Among adults, a slight male predominance exists, with reported male-to-female ratios ranging from 1.25:1 to 1.7:1 depending on the clinical setting.

Geographic and Aetiological Variation

• In high-income countries, malignancy—particularly lung and breast cancer—is now the most common cause of pericardial tamponade.
• Purulent pericarditis and uraemic effusions are also associated with higher incidence.
• In regions where tuberculosis is endemic, tuberculous pericarditis remains a leading cause of pericardial effusion progressing to tamponade.
• Tamponade complicating acute idiopathic pericarditis is comparatively rare.

Demographic Risk Patterns

• Younger adults are more likely to present with tamponade secondary to trauma or HIV-associated pericarditis.
• Elderly individuals are more often affected when tamponade is related to malignancy or chronic renal failure.

• History of breast or lung cancer, metastatic disease, or prior chemotherapy/radiotherapy increases risk.
• Up to 60% of effusions in malignancy are therapy-related rather than direct tumour spread.

Renal failure

• Suggests uraemic pericarditis and effusion.
• Tamponade occurs in up to 20% of dialysis-related cases.

Autoimmune or connective tissue disease

• Past medical history of systemic lupus erythematosus, rheumatoid arthritis, or dermatomyositis may point towards an immune-mediated cause.

Hypothyroidism

• Long-standing untreated hypothyroidism can cause gradual effusion development, though tamponade is rare.

Recent myocardial infarction

• Raises concern for free wall rupture.
• Dressler syndrome may also result in tamponade.

Aortic dissection

• Tamponade is a recognised and often fatal complication of acute type A dissections.

Tuberculosis

• Particularly relevant in endemic areas or in patients with HIV.
• May present with systemic features such as night sweats, fever, and weight loss.

Iatrogenic causes

• History of cardiac surgery, valve replacement, or coronary intervention.
• Procedures such as ablation, pacemaker/defibrillator lead placement, or central venous catheterisation can all precede tamponade.

Drugs

• Exposure to agents such as hydralazine, procainamide, isoniazid, or minoxidil may induce drug-related lupus with pericardial effusion.

Radiation exposure

• Prior mediastinal or chest wall irradiation for malignancy is a recognised risk factor.

Other procedures/trauma

• Acupuncture, chest trauma, and oesophagogastric surgery have all been implicated.
  
  

Risk Stratification from History

Strong associations

• Malignancy (particularly lung and breast)
• Aortic dissection
• Purulent pericarditis
• Large idiopathic chronic effusion
• Recent cardiac surgery/intervention
• Tuberculosis

Weaker associations

• Autoimmune disease
• Hypothyroidism
• Uraemia
• Anticoagulation therapy

Tachycardia

• Seen in nearly all patients as a compensatory mechanism for reduced stroke volume.
• Reported in up to 88% of cases, with pooled sensitivity of 77% (95% CI 69–85%).
• May be absent in hypothyroidism-associated tamponade or early tamponade despite significant effusion.

Hypotension

• Reflects failure of compensatory tachycardia.
• Occurs in approximately 35% of non-traumatic tamponade cases.
• Pooled sensitivity is low at 26% (95% CI 16–36%).

Elevated jugular venous pressure (JVP)

• Nearly universal in tamponade, often with venous distension visible in neck, forehead, or scalp.
• Preserved x descent with absent or attenuated y descent due to impaired ventricular filling.
• Sensitivity estimated at 76% (95% CI 62–90%).
• Absent in low-pressure tamponade associated with hypovolaemia.

Distant or muffled heart sounds

• Caused by fluid dampening cardiac acoustic transmission.
• One of Beck’s triad but with low sensitivity (~28%).

Pericardial friction rub

• More common in inflammatory aetiologies.
• May be absent in large effusions where pericardial layers are separated.

Hepatomegaly

• Present in over half of patients due to systemic venous congestion.

Cold, clammy skin and weak pulse

• Result from systemic hypoperfusion and shock.

Beck’s triad

• Hypotension, raised JVP, and muffled heart sounds.
• Classically described in acute tamponade but only present in a minority of non-traumatic cases.

Pulsus paradoxus

• Defined as a fall in systolic blood pressure >10 mmHg on inspiration.
• Sensitivity estimated at 82% (95% CI 72–92%), positive likelihood ratio 3.3.
• Represents exaggerated ventricular interdependence during inspiration.
• Absent in certain conditions: atrial septal defect, aortic regurgitation, severe pulmonary hypertension, acute LV ischaemia, RV dysfunction, or low-pressure tamponade.

Kussmaul sign

• Paradoxical rise in JVP on inspiration.
• Rare in tamponade, more commonly seen in constrictive pericarditis or effusive-constrictive disease.

Ewart sign

• Dullness to percussion with bronchial breath sounds and bronchophony below the left scapula.
• Occurs in large pericardial effusions.

The y descent

• Typically abolished in tamponade due to impaired ventricular diastolic filling.

Dysphoria

• Agitation, unusual behaviour, or sense of impending death reported in up to 26% of patients.

Low-pressure tamponade

• Seen in hypovolaemic patients or those with large but slowly accumulating effusions.
• Classical findings (tachycardia, pulsus paradoxus, raised JVP) may be absent.
• Identified in 10–20% of large effusions.

Approach Considerations

• Cardiac tamponade should be suspected on clinical grounds, but laboratory, imaging, and haemodynamic studies are used to support the diagnosis.
• Echocardiography is the first-line test and should be performed without delay.
• The European Society of Cardiology (ESC) Working Group on Myocardial and Pericardial Diseases has proposed a scoring system combining clinical, imaging, and aetiological parameters.
  • Score ≥6 → immediate pericardial drainage.
  • Score <6 → drainage may be delayed safely for 12–48 hours.

Echocardiography

• Primary diagnostic tool for tamponade.
• Typical findings include:
  • Echo-free space around the heart (pericardial effusion).
  • Early diastolic collapse of the right ventricular free wall.
  • Late diastolic collapse of the right atrium.
  • Swinging motion of the heart within the effusion.
  • Apparent left ventricular pseudohypertrophy.
  • Plethoric inferior vena cava with little/no inspiratory collapse.
  • Doppler evidence of exaggerated respiratory variation in flow:
    • 40% augmentation across tricuspid inflow.
    • 25% inspiratory decrease in mitral inflow.
• Mimics that may simulate effusion include pleural effusion, mediastinal masses, calcification, aneurysms, or catheters within the heart.

Laboratory Studies

Creatine kinase and isoenzymes

• Elevated in myocardial infarction and cardiac trauma.

Renal profile and full blood count (FBC)

• Identify uraemia, infection, or anaemia in chronic disease.

Coagulation profile

• Determines bleeding risk prior to pericardiocentesis or surgery.

Autoimmune screening (ANA, ESR, rheumatoid factor)

• May suggest an underlying connective tissue disorder.

HIV testing

• Effusions are associated with HIV in approximately 24% of cases.

Tuberculosis screening (PPD)

• Particularly important in endemic areas.

Imaging Studies

Chest radiography

• May show cardiomegaly and a classic “water bottle” silhouette.
• Pericardial calcifications or chest wall trauma may be seen.
• In children, a bowed catheter on X-ray can suggest tamponade after central line insertion.

Computed tomography (CT)

• Useful in complex or postoperative cases.
• Can demonstrate compression of the coronary sinus, an early marker.
• Provides excellent definition of pericardial anatomy and dynamics.

Magnetic resonance imaging (MRI)

• Highly sensitive, detecting effusions as small as 30 mL.
• Offers detailed assessment of pericardial thickness and ventricular interaction.
• Limited use in emergencies due to timing.

Electrocardiography

Sinus tachycardia

• Common but non-specific finding.

Low-voltage QRS complexes

• Suggest large pericardial effusion or tamponade.

Electrical alternans

• Alternating QRS amplitude due to swinging motion of the heart.
• Strongly suggestive but not pathognomonic.

PR segment depression

• May accompany pericarditis-related effusions.

Pulse Oximetry

• Shows respiratory variability in waveform in patients with pulsus paradoxus.
• Particularly useful in atrial fibrillation, where BP measurement is unreliable.

Swan-Ganz Catheterisation

• Demonstrates near equalisation of right atrial, right ventricular diastolic, pulmonary arterial diastolic, and wedge pressures.
• Right atrial tracings show a preserved x descent with absent y descent.
• Useful in differentiating tamponade from constrictive pericarditis or restrictive cardiomyopathy.

Histological and Cytological Studies

Pericardial biopsy

• Indicated when effusion aetiology is unclear (e.g., suspected tuberculosis).
• Granulomas may be observed in tuberculous pericarditis.

Pericardial fluid analysis

• Cytology and culture identify the cause in ~75% of non-traumatic cases.
• Particularly valuable for detecting malignancy or bacterial infection.

Pleural effusion

• Large effusions can impair cardiac filling by increasing intrathoracic pressure.
• Clinical findings may overlap with tamponade, including dyspnoea and reduced cardiac output.
• Imaging distinguishes pleural from pericardial fluid collections.

Pneumothorax

• Both tension pneumothorax and tamponade can present with hypotension, jugular venous distension, and muffled heart sounds.
• Pneumothorax produces absent breath sounds and hyperresonance on percussion, features absent in tamponade.
• Chest radiography rapidly distinguishes the two.

Pulmonary embolism

• May present with dyspnoea, hypotension, tachycardia, and raised jugular venous pressure.
• Right ventricular strain is seen on echocardiography, but without pericardial effusion or chamber collapse.
• CT pulmonary angiography is diagnostic.

Heart failure

• Both conditions cause venous congestion, hepatomegaly, and peripheral oedema.
• In heart failure, pulmonary rales and elevated BNP are more typical.
• Echocardiography shows poor ventricular function rather than effusion-related collapse.

Shock (nonspecific)

• Obstructive or cardiogenic shock can mimic tamponade clinically.
• Echocardiography is decisive, identifying the presence or absence of pericardial effusion and haemodynamic compromise.

Key Mimics

Constrictive pericarditis

• Often follows radiation therapy, recurrent pericarditis, or cardiac surgery.
• Presents with Kussmaul’s sign: rise in jugular venous pressure with inspiration (usually absent in tamponade).
• Echocardiography: thickened pericardium without effusion, rapid early diastolic filling with impaired late filling.
• CT/MRI: demonstrates pericardial thickening and calcification.
• Invasive haemodynamics: steep y-descent with “dip and plateau” or square root sign, unlike tamponade where the y-descent is blunted.

Effusive-constrictive pericarditis

• Combines features of effusion and constriction.
• Echocardiography shows pericardial effusion with features of constriction.
• Tamponade physiology may persist after fluid drainage.

Restrictive cardiomyopathy

• Produces raised venous pressures and Kussmaul’s sign.
• Differentiated by absence of effusion.
• Associated features: left ventricular hypertrophy, atrial enlargement, pulmonary hypertension, and absence of respiratory variation in filling.
• Echocardiography and MRI are useful for distinction.

Cardiogenic shock

• Mimics tamponade with hypotension, tachycardia, and elevated jugular venous pressure.
• Echocardiography demonstrates poor global ventricular function or regional wall motion abnormalities.
• Absence of pericardial effusion and chamber collapse excludes tamponade.

General Principles

• Urgent drainage of pericardial fluid is the definitive treatment.
• Echocardiography-guided pericardiocentesis is first-line in most cases without trauma, haemopericardium, or purulent effusion.
• Surgical drainage is preferred for traumatic, purulent, or haemorrhagic tamponade, and when percutaneous approaches are contraindicated.
• Patients must be monitored in an intensive care setting for recurrence and complications such as pericardial decompression syndrome.

Supportive Measures

Intravenous fluids

• Useful in hypovolaemic patients as a temporising measure.
• Can variably increase cardiac output but may worsen filling pressures in some patients.

Avoid inotropes, vasodilators, and diuretics

• Ineffective in tamponade physiology and may aggravate haemodynamic compromise.

Avoid positive-pressure ventilation

• Increases intrathoracic pressure and further reduces venous return and cardiac filling.

Bed rest with leg elevation

• Can transiently augment venous return and provide short-term improvement.

Oxygen therapy

• Provides supportive benefit in all patients with compromised haemodynamics.

Pericardial Drainage

Pericardiocentesis

• First-line therapy in most unstable patients without traumatic or purulent effusion.
• Performed under echocardiographic or fluoroscopic guidance.
• Landmark-guided subxiphoid approach may be used in extreme emergencies when imaging is unavailable.
• Complications include myocardial or coronary laceration, arrhythmias, pneumothorax, and liver injury (1–2% incidence with imaging guidance).
• Contraindicated in aortic dissection; relatively contraindicated in severe coagulopathy.
• A catheter should remain in situ until drainage is <25 mL/day.

Surgical drainage

• Indicated for tamponade caused by trauma, haemopericardium, or purulent effusion.
• Options include:
  • Subxiphoid pericardiotomy: Direct visualisation with controlled drainage.
  • Pericardial window (thoracoscopic or open): Allows decompression into pleural space; reduces recurrence risk.
  • Balloon pericardiotomy: Minimally invasive alternative with good short-term outcomes.
  • Thoracotomy/sternotomy: Required for type A aortic dissection, ventricular rupture, or penetrating trauma.
  • Pericardiectomy or pericardio-peritoneal shunt: Reserved for recurrent or refractory effusions, especially malignant.

Aetiology-Specific Management

Pericarditis (viral/idiopathic)

• NSAIDs and colchicine reduce recurrence after drainage.
• Corticosteroids or IL-1 inhibitors (e.g., anakinra, rilonacept) may be considered in refractory cases.

Purulent pericarditis

• Requires urgent surgical drainage and intravenous antibiotic therapy.
• Associated with high mortality if untreated.

Malignancy

• May result from tumour infiltration, radiotherapy, or chemotherapy.
• Often requires definitive surgical drainage or window creation to prevent recurrence.

Trauma or haemopericardium

• Managed surgically, often via thoracotomy or sternotomy to repair bleeding sites.

Monitoring and Follow-Up

Post-procedural monitoring

• Continuous telemetry and frequent haemodynamic checks for at least 24–48 hours.
• Repeat echocardiography before discharge, at 1–2 weeks, and again at 6–12 months depending on recurrence risk.

Long-term prevention

• Catheter drainage reduces recurrence.
• Malignant effusions may require pericardial window or sclerotherapy.
• Inflammatory effusions may be prevented with anti-inflammatory therapy.

Impact of Timely Intervention

• Prognosis worsens with delays in recognition and treatment.
• Re-exploration for tamponade after cardiac surgery is associated with increased morbidity and mortality.
• Adverse outcomes are largely related to complications of delayed intervention such as blood loss and transfusion requirements.

Post-Surgical Considerations

• Placement of multiple mediastinal chest tubes does not reduce the risk of reoperation compared with a single drain.
• Surgical strategies should be tailored to individual patient risk rather than routine multiple drainage tubes.

Prognosis by Underlying Aetiology

• Malignancy: One-year mortality >75%, with median survival ~150 days.
• Acute myocardial infarction with free wall rupture: Mortality 70–100%.
• Aortic dissection: Mortality around 65%.
• Haemopericardium due to bleeding/anticoagulation: Mortality ~40%.
• Infectious/inflammatory causes: Mortality ~8%.
• Iatrogenic causes: Mortality ~10%.

Importance of Treating the Underlying Cause

• Pericardial drainage alone is lifesaving but insufficient for long-term prognosis.
• Addressing the primary aetiology (malignancy, dissection, infection, etc.) is crucial to prevent recurrence and improve survival.

Cardiac Arrest

• Represents the final stage of untreated or unrecognised tamponade.
• Sudden cardiovascular collapse occurs if drainage is delayed, often leading to death unless urgent intervention is undertaken.

Death

• Mortality rates are strongly influenced by the underlying cause.
• Reported in-hospital mortality:
  • Acute myocardial infarction with free wall rupture: 70–100%.
  • Aortic dissection: ~65%.
  • Haemorrhage/anticoagulation: ~40%.
  • Malignancy: ~16%, with 12-month mortality approaching 80%.
  • Iatrogenic: ~10%.
  • Infectious/inflammatory causes: ~8%.

Cardiogenic Shock

• Severe haemodynamic compromise may present as cardiogenic shock.
• Prolonged systemic hypoperfusion can lead to multi-organ dysfunction, particularly renal failure.

Recurrent Pericardial Effusion

• Risk of recurrence is influenced by the cause of the effusion, with malignant disease being the strongest predictor.
• Effusion may reaccumulate even after initial drainage due to closure of pericardial windows or catheter tracts.
• Approximate recurrence rates:
  • Pericardiocentesis: ~50%.
  • Surgical drainage: 10–20%.
• Adequate treatment of the underlying condition reduces recurrence risk.

Pericardial Decompression Syndrome (PDS)

• A rare but serious complication occurring after rapid fluid removal.
• Manifests as paradoxical haemodynamic collapse and/or acute pulmonary oedema following drainage.
• Patients should be observed in an intensive care unit for early detection and treatment.

1. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964.
2. Alerhand S, Adrian RJ, Long B, et al. Pericardial tamponade: a comprehensive emergency medicine and echocardiography review. Am J Emerg Med. 2022;58:159-174.
3. Antman EM, Cargill V, Grossman W. Low-pressure cardiac tamponade. Ann Intern Med. 1979;91(3):403-406.
4. Boltwood CM, Skorton DJ, Collins SM, et al. Inspiratory traction sign: a new finding in pericardial tamponade. Am J Cardiol. 1983;51(5):902-906.
5. Brucato A, Imazio M, Gattorno M, et al. Effect of anakinra on recurrent pericarditis among patients with colchicine resistance and corticosteroid dependence: the AIRTRIP randomized clinical trial. JAMA. 2016;316(18):1906-1912.
6. Cornily JC, Pennec PY, Castellant P, et al. Cardiac tamponade in medical patients: a 10-year follow-up survey. Cardiology. 2008;111(3):197-201.
7. Goldstein JA. Cardiac tamponade in the postoperative period. J Am Coll Cardiol. 2010;55(15):1647-1652.
8. Haneya A, Philipp A, Diez C, et al. Reexploration for bleeding or tamponade after cardiac surgery. Ann Thorac Surg. 2012;94(2):503-509.
9. Hancock EW. Subacute effusive-constrictive pericarditis. Circulation. 1971;43(2):183-192.
10. Kearns MJ, Walley KR. Tamponade: haemodynamic and echocardiographic diagnosis. Chest. 2018;153(5):1266-1275.
11. 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(9):965-1012.
12. Klein AL, Imazio M, Cremer P, et al. RHAPSODY: Rilonacept in recurrent pericarditis. N Engl J Med. 2021;384(1):31-41.
13. Klopfenstein HS, Schuchard H, Wann LS, et al. The relative merits of pulsus paradoxus and right ventricular diastolic collapse in the early detection of cardiac tamponade. Circulation. 1985;71(4):829-833.
14. Le Guillou V, Langanay T, Verhoye JP, et al. Multiple versus single chest tube drainage after cardiac surgery: impact on reoperation for bleeding and tamponade. Interact Cardiovasc Thorac Surg. 2012;14(5):562-566.
15. LeWinter MM, Kabbani S. Pericardial diseases. In: Zipes DP, Libby P, Bonow P, et al. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. Philadelphia: WB Saunders; 2005:1757-1781.
16. Monaco F, Testa L, Riva G, et al. Video-assisted thoracoscopic pericardial window for cardiac tamponade: feasibility and outcomes. Eur J Cardiothorac Surg. 2015;47(2):e52-e57.
17. Reddy PS, Curtis EI, O'Toole JD, et al. Cardiac tamponade: haemodynamic observations in man. Circulation. 1978;58(2):265-272.
18. Roy CL, Minor MA, Brookhart MA, et al. Does this patient with a pericardial effusion have cardiac tamponade? JAMA. 2007;297(16):1810-1818.
19. Sagristà-Sauleda J, Angel J, Sambola A, et al. Effusive-constrictive pericarditis. N Engl J Med. 2004;350(5):469-475.
20. Sagristà-Sauleda J, Angel J, Sambola A, et al. Low-pressure cardiac tamponade: clinical and haemodynamic profile. Circulation. 2006;114(9):945-952.
21. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690.
22. Stone JR, Basso C, Baandrup UT, et al. Recommendations for processing cardiovascular surgical pathology specimens: a consensus statement. Cardiovasc Pathol. 2012;21(1):2-16.