Pericardial disease

This CCC will cover pericarditis, cardiac tamponade, pericardial effusion.

🦴 Anatomy

The pericardium is a fibro-serous sack surrounding the heart and roots of the great vessels.

It is made up of 2 main layers:

1. Fibrous pericardium - tough outer external layer that is continuous with the central tendon of the diaphragm.
2. Serous pericardium - can be further divided into 2 layers:
1. Parietal layer - lines the internal surface of the fibrous pericardium.
2. Visceral layer - lines the external surface of the heart (this is also known the epicardium).
3. Between the 2 layers there is a cavity containing serous fluid which minimises friction as the heart contracts.

The phrenic nerve (C3-C5) is responsible for the somatic innervation of the pericardium. It is a common source of referred pain, for example, having shoulder pain experienced as a result of pericarditis.

PERICARDITIS

Pericarditis is the inflammation of the pericardium.

🔢 Classification

Before discussing the pathophysiology and aetiology of the disease, let’s discuss how we classify the disease as the aetiologies may differ depending on the type of pericarditis.

It is classified based on its timing:

We will be looking at acute pericarditis and constrictive pericarditis.

🫀 Acute pericarditis

Acute pericarditis is the new-onset of pericarditis lasting <4-6 weeks.

Pathophysiology

It is mostly either due to idiopathic causes or viral infection. These 2 make up 90% of cases.

😷 Presentation

🔍 Investigations

1. 🥇 Echocardiography
2. 🥇 ECG - may show global and widespread changes on ECG. There are some specific markers such as :
1. Concave ST elevation
2. PR depression throughout the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-V6)
3. 🥇 Bloods
1. CRP elevated as it is a marker of inflammatory.
2. Troponin is elevated in 1/3rd of patients, indicating myopericarditis.

🧰 Management

It is important to treat the underlying cause.

If idiopathic or due to viral causes, we can use NSAIDs and colchicine (colchicine also works as an anti-inflammatory and is given for 3-6 months to prevent recurrence).

🫀 Constrictive pericarditis

Constrictive pericarditis is the persistent inflammation of the pericardium >3 months due to fibrous thickening of the pericardium → impaired diastolic ventricular filling because of the decreased elasticity as a result.

Pathophysiology

It is usually idiopathic but can occur due to any cause of pericarditis. Once again TB is the most common cause in developing countries.

😷 Presentation

• Dyspnoea
• Right heart failure - resulting in a raised JVP, ascites, oedema and hepatomegaly. Shows prominent X and Y descent on JVP waveform.
• Pericardial knock - a third heart sound that is high-pitched and made by the heart in early diastole when ventricular filling is suddenly halted by the restraining pericardium.
• Positive Kussmaul’s sign - a paradoxical raise in JVP on inspiration (normally decreases on inspiration).

🔍 Investigations

1. Echocardiography is the gold standard.
2. ECG similar to what we saw in acute pericarditis with concave ST elevation and PR depression.
3. Bloods - with raised CRP, troponin again.
4. CXR - showing pericardial calcification or pericardial effusion

🧰 Management

• Pericardiectomy - removal of the entire or portions of the pericardium.

Management of the underlying cause is also necessary, for example management of TB.

CARDIAC TAMPONADE

Cardiac tamponade occurs when there is a rapid accumulation of fluid within the pericardial activity thus increasing the intra-pericardial cavity pressure → preventing heart from expanding during diastole → decreased ventricular filling and decreased cardiac output. Essentially, it is a rapid pericardial effusion in which the heart has no time to adjust and accommodate.

It is a life-threatening disease needing immediate management otherwise it can lead to cardiac arrest.

It occurs often due to iatrogenic causes (after surgery or cardiac interventions). It may also be due to other causes of pericardial effusion/pericarditis such as viral infection, connective tissue disorders, TB, thoracic trauma. Malignancy is another cause.

😷 Presentation

• Dyspnoea
• Tachycardia
• Chest pain
• Abdominal pain
• Confusion
• Absent Y descent on JVP waveform
• Beck’s triad
1. Muffle heart sounds
2. Hypotension
3. Raised JVP

• Pulsus paradoxus - with stretching the pericardium, the ventricular filling with inspiration is exaggerated between the left and right ventricles. Inspiration increases the negative intra-thoracic pressure and increases venous return to the right-hand side of the heart. This pushes the interatrial and interventricular septum Into the left heart (ventricular interdependence) which decreases its filling capacity → decreasing cardiac output.

Simply put pulsus paradoxus is a drop in systemic blood pressure >10mmHg on inspiration.

🔍 Investigations

• Transthoracic echocardiogram - this is the gold-standard investigation. It will show fluid around the heart and ventricular compromise.
• ECG - low-voltage (low-amplitude) QRS complexes ± electrical alternans (tall and short QRS complexes in intervals ).
• Electrical alternans occurs when the heart swings backwards and forwards within a large fluid-filled pericardium, thus causing the electrical activity to travel towards a wandering base-line.
• CXR - shows large globular heart.

🧰 Management

💉

Drainage:

• Haemodynamic instability - if the systolic BP <100mmHg or there is pulsus paradoxus >10mmHg → urgent pericardiocentesis using subxiphoidal approach.
• Complications include: pneumothorax, damage to myocardium and coronary vessels, thrombus, arryhthmias/cardiac arrest.
• Haemopericardium or associated malignancy or traumatic/purulent effusion → surgical drainage.

Constrictive pericarditis vs cardiac tamponade

PERICARDIAL EFFUSION

Pericardial effusion is the accumulation of fluid within the pericardial space above the normal volume. The normal volume is usually 15-50mL. It can present acutely or may be due to chronic effusion.

1. Acute pericardial effusion - a sudden, critical rise in intra-pericardial pressure that then applies pressure on the heart. In acute cases, the pericardial cavity only accommodates 100-250mL of fluid.
2. Chronic pericardial effusion - may happen over weeks-months, and such the pericardium has the ability to stretch and accommodate, allowing for 1-2L of fluid being held within the cavity.

⚠️ Risk factors and causes

😷 Presentation

1. Dyspnoea
2. Chest pain
3. Ewart’s sign - compression of the left lower lung base leading to bronchial breathing (when auscultating the inferior angle of the left scapula), egophony and dullness when percussing over the lateral side of the left scapula.
4. Nausea
5. Muffled heart sounds
6. Signs of cardiac tamponade - such as raised JVP, chest pain, hypotension etc.

🔍 Investigations

• CXR - if the effusion is >300mL the CXR will show enlarged globular heart.
• ECG - will show low-voltage QRS complexes ± electrical alternans.
• Echocardiography - may show regions of reduced echogenicity (echo-free zones) surrounding the heart.
• Pericardiocentesis - may be diagnostic in suspected bacterial pleural effusions.

🧰 Management

Treat the underlying cause.

Pericardiocentesis is therapeutic in cardiac tamponade.