Pericardial Effusion and Cardiac Tamponade

Introduction

The pericardium is a double-layered sac surrounding the heart, normally containing 15-50 ml of serous fluid that lubricates cardiac motion. The parietal layer is fibrous and relatively non-compliant in the short term, and this single anatomical fact explains almost everything about tamponade.¹

Because the sac cannot stretch quickly, the rate of accumulation matters far more than the volume. As little as 150-200 ml accumulating rapidly - after cardiac perforation during a procedure, or in penetrating trauma - can cause fatal tamponade. Conversely, 1-2 litres accumulating slowly over months, as in a malignant or hypothyroid effusion, may be entirely asymptomatic because the pericardium has had time to stretch.

Once the pericardial reserve volume is exhausted, the pressure-volume curve becomes almost vertical: each additional millilitre of fluid causes a steep rise in intrapericardial pressure. This is why a patient with a chronic effusion can deteriorate abruptly from stable to peri-arrest with little apparent change.

Aetiology

Clinical features

Symptoms

• Breathlessness - the commonest symptom, often progressive and worse lying flat
• Chest discomfort - a dull ache or pressure, or pleuritic pain if there is associated pericarditis
• Fatigue and reduced exercise tolerance
• Presyncope and dizziness - from falling cardiac output
• Cough, hoarseness, hiccups or dysphagia - from compression of adjacent structures by a large effusion
• Symptoms of the underlying cause - fever, weight loss, night sweats, malignancy, renal failure
• Asymptomatic - large chronic effusions may be found incidentally on imaging

Signs of tamponade

• Tachycardia - an early and near-universal compensatory sign. Its absence in a hypotensive patient should prompt consideration of hypothyroidism or beta-blockade.
• Pulsus paradoxus - a fall in systolic blood pressure of more than 10 mmHg on inspiration. Measure it by inflating a manual cuff above systolic and deflating slowly: note the pressure at which Korotkoff sounds are first heard (in expiration only), then the pressure at which they are heard throughout the respiratory cycle. The difference is the paradox.
• Raised JVP with a prominent x descent and absent y descent - filling occurs during ventricular systole but not in early diastole, because the pericardium is already full
• Kussmaul's sign - a paradoxical rise in JVP on inspiration. It is characteristic of constrictive pericarditis and is typically absent in tamponade, which is a useful discriminator.
• Cool peripheries, prolonged capillary refill, oliguria and confusion - signs of shock
• Ewart's sign - dullness to percussion with bronchial breathing below the left scapula, from compression of the left lower lobe by a large effusion
• Impalpable apex beat and a pericardial rub, which may persist even with a large effusion

Investigations

ECG

• Sinus tachycardia - almost always present
• Low voltage QRS complexes - under 5 mm in the limb leads or 10 mm in the chest leads, as fluid attenuates the electrical signal
• Electrical alternans - beat-to-beat alternation in QRS amplitude, caused by the heart physically swinging within the fluid. It is highly specific for a large effusion with tamponade but not sensitive, so its presence is very useful and its absence means little.
• Widespread saddle-shaped ST elevation with PR depression - if there is associated pericarditis
• Pulseless electrical activity - the terminal event

Echocardiography

The investigation of choice, available at the bedside, and both diagnostic and therapeutic when used to guide drainage.

• An echo-free space surrounding the heart, with the size and distribution described (circumferential or loculated)
• Diastolic collapse of the right atrium - the earliest and most sensitive sign of raised intrapericardial pressure
• Diastolic collapse of the right ventricle - more specific for haemodynamically significant tamponade
• A dilated inferior vena cava with less than 50% inspiratory collapse - reflecting raised venous pressure
• Exaggerated respiratory variation in mitral and tricuspid inflow velocities - the echocardiographic equivalent of pulsus paradoxus
• Septal bounce and a swinging heart within a large effusion

Other investigations

• Chest X-ray - a globular, flask-shaped or water-bottle cardiac silhouette, though this requires an effusion of at least 200-300 ml. Clear lung fields with a large heart is a useful pattern, distinguishing it from heart failure.
• Bloods - FBC, U&Es (uraemia), CRP and ESR, thyroid function, troponin, blood cultures, autoimmune screen, and a coagulation screen before drainage
• CT or cardiac MRI - better for loculated and posterior effusions, for pericardial thickening, and for staging malignancy
• Pericardial fluid analysis at drainage - protein and LDH (Light's criteria for exudate versus transudate), cell count and differential, microscopy, culture and sensitivity including TB culture and PCR, adenosine deaminase (raised in tuberculous pericarditis), and cytology for malignant cells

Management

The stable effusion without tamponade

• Treat the underlying cause - NSAIDs and colchicine for inflammatory pericarditis, dialysis for uraemic effusion, levothyroxine for hypothyroidism, antituberculous therapy for TB, antibiotics for purulent pericarditis
• Serial echocardiography to monitor size and the development of tamponade physiology
• Diagnostic pericardiocentesis where the cause is unclear and analysis of the fluid would change management, particularly where tuberculosis or malignancy is suspected
• Consider drainage of a large effusion (over 20 mm on echocardiography) even without tamponade, given the risk of progression and the diagnostic value

Cardiac tamponade

Pericardiocentesis

Performed under echocardiographic guidance wherever possible, which has largely superseded the blind subxiphoid approach and has substantially reduced complications.^1,7 A needle is advanced towards the largest fluid pocket, position is confirmed with agitated saline contrast, and a guidewire and pigtail catheter are placed by the Seldinger technique.

Complications include cardiac chamber or coronary artery laceration, pneumothorax, arrhythmia, hepatic injury and infection. Pericardial decompression syndrome - acute ventricular dysfunction and pulmonary oedema after rapid drainage of a large effusion - is rare but recognised, and is one reason drainage may be staged rather than complete in a single sitting.

Recurrent effusions

• Prolonged catheter drainage until output falls below approximately 25-50 ml per day
• Pericardial window - a surgically created communication between the pericardium and the pleural or peritoneal space, allowing continuous drainage
• Balloon pericardiotomy - a percutaneous alternative in malignant effusion
• Intrapericardial sclerosing or chemotherapeutic agents - occasionally used in malignant effusion
• Pericardiectomy - for constrictive pericarditis or refractory recurrent effusion
• Colchicine - reduces recurrence in inflammatory pericarditis⁵

Constrictive pericarditis

An important related condition in which a thickened, fibrosed and often calcified pericardium restricts diastolic filling. It commonly follows tuberculous, purulent or radiation pericarditis, or cardiac surgery, and may develop after any cause of pericardial inflammation.

Constriction must also be distinguished from restrictive cardiomyopathy, which produces similar haemodynamics but is a myocardial rather than a pericardial disease, and is not surgically treatable. Cardiac MRI, tissue Doppler and, where necessary, invasive haemodynamic study are used to separate them.

Red flags

Prognosis

Prognosis is determined almost entirely by the underlying cause rather than by the effusion itself, provided tamponade is recognised and drained promptly.

Idiopathic and viral effusions usually resolve completely, and small effusions found incidentally in an otherwise well patient rarely progress. Uraemic and hypothyroid effusions resolve with treatment of the underlying condition.

Malignant pericardial effusion carries a poor prognosis, with median survival typically measured in a few months, reflecting the advanced disease it signifies rather than the effusion itself. Recurrence after drainage is common, which is why a pericardial window is often preferred over repeated aspiration.

Tuberculous pericarditis responds to antituberculous therapy but carries a significant risk of progression to constrictive pericarditis, and requires prolonged follow-up.⁶ Purulent pericarditis has a high mortality without prompt surgical drainage and antibiotics.

Untreated cardiac tamponade is uniformly fatal, but the response to drainage can be immediate and dramatic. It is one of the small number of conditions in medicine where a correct diagnosis and a single procedure convert a dying patient into a well one within minutes - which is precisely why the clinical signs are worth knowing thoroughly.