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Ashley EA, Niebauer J. Cardiology Explained. London: Remedica; 2004.

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Cardiology Explained.

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Chapter 13Pericardial disease


A diagnosis of pericarditis (inflammation of the pericardium), though rare, should always be considered as a differential for ischemic heart pain. The key differentiating features are that the pain in pericarditis is altered by posture and can be exacerbated by deep inspiration. Classically, the patient will be found sitting forward and taking shallow breaths.


The pericardium has two layers: visceral and parietal. The visceral layer is closely apposed to the heart, whilst the fibrous parietal layer provides a more rigid outer shell to the pericardial cavity (see Figure 1). The normal volume of pericardial fluid is in the region of 50 mL.

Figure 1. The layers of pericardium.

Figure 1

The layers of pericardium. The visceral pericardium is a tissue paper-like layer, while the parietal pericardium is more rigid.

The causes of pericarditis are outlined in Table 1. Viral pericarditis is the most common type, but in many cases either the diagnosis is never made or the viral infection is never identified. Another common presentation is characteristic pain 3–14 days postmyocardial infarction (MI) or postcardiac surgery, which tends to be self-limiting. Relapsing episodes are referred to as Dressler's syndrome or postcardiotomy syndrome, and are thought to represent an autoimmune process.

Table 1. Causes of pericarditis.

Table 1

Causes of pericarditis.



Auscultation may reveal a pericardial rub, which is sufficient, but not necessary, to make the diagnosis. It can easily be distinguished from a pleural rub by asking the patient to hold their breath.


The classic sign of pericarditis – a concave upwards ("saddle") ST-segment elevation throughout the 12 leads – is, of course, rare. However, some form of electrocardiogram (ECG) abnormality is common. These changes are either present in all 12 leads or in leads that do not correspond to the territory perfused by a single coronary artery. Low voltages suggest the possibility of effusion.

Chest x-ray

A chest x-ray (CXR) can help to rule out a tuberculous cause of pericarditis and exclude significant effusion.


Echocardiography is helpful mainly if there is a suspicion of effusion or tamponade.

Blood tests

Blood tests for immune markers, such as the antinuclear cytoplasmic antibody (ANCA), should be carried out in any patient with confirmed pericarditis. Acute and convalescent viral titers can also be requested, but rarely alter management.


Nonsteroidal anti-inflammatory drugs are the treatment of choice for pericarditis. They relieve both the inflammatory process and the pain. Steroids may be required in serositic pericarditis, whereas pericarditis with a suspicious CXR and constitutional symptoms should prompt investigation for tuberculosis.

Pericardial effusion and tamponade

As with pleural effusion, the key defining presentation of pericardial effusion is the rate of fluid accumulation. Any cause of pericarditis can result in a significant accumulation of serous fluid, while hemopericardium (a collection of blood in the pericardial sac surrounding the heart) can be caused by trauma, type 1 dissection of the aorta, and cardiac rupture. The key feature is not the overall volume of fluid (even hundreds of milliliters can be asymptomatic if accumulated over a long enough time), but the rate of rise – as with pleural effusion, removal of even a small amount of fluid can result in significant benefit.

Small, asymptomatic effusions can often be left to resorb on their own. This usually requires repeat echo at regular intervals to ensure that resorption has occurred. Larger effusions bounded by the tough parietal pericardium can compromise the low pressure right heart – this results in tamponade (see Figure 2).

Figure 2. An extreme form of pericardial effusion, known as a "swinging heart".

Figure 2

An extreme form of pericardial effusion, known as a "swinging heart". The arrow indicates the effusion.


Cardiac tamponade is a medical emergency. It is associated with a characteristic jugular venous pressure (JVP). Kussmaul's sign describes a raised JVP that rises further on inspiration, while Friedrich's sign describes a steep x/y descent (although, in reality at the bedside, the waves are hard to discern). The heart sounds are quiet and there may be a rub.

Kussmaul's Legacy

Adolph Kussmaul was Professor of Medicine successively at Heidelberg, Erlangen, Freiburg, and Strasbourg. As well as describing the paradoxical increase in JVP on inspiration in patients with restrictive cardiomyopathy, right ventricular failure, and constrictive pericarditis, he described the deep-sighing respiration associated with low arterial pH (Kussmaul breathing) and coined the term "polyarteritis nodosa". In fact, Kussmaul's JVP sign is widely misunderstood to be solely the result of right ventricular incompliance, when in fact the explanation relates as much to distension of the mesenteric vascular bed and the change from a right ventricular pressure that predominantly reflects negative intrapleural pressure "sucking" blood into the chest, to one that predominantly reflects positive intra-abdominal pressure "pushing" the greater volume proximally.

A characteristic of cardiac tamponade is pulsus paradoxus, which is not paradoxical at all, but an exaggeration of the normal drop in systolic pressure on inspiration –>10 mm Hg is abnormal. To test for it, inflate the cuff to just above systolic pressure then slowly deflate, stopping each 5 mm Hg for a full inspiration–expiration cycle. Listen for the point at which the beating becomes continuous throughout the breathing cycle.


Low-voltage ECG and beat-to-beat variation in R-wave amplitude are characteristic.

Chest x-ray

CXRs show a globular, "boot-shaped" heart.


Echo is the investigation of choice. The key observation is diastolic collapse of the right atrium and ventricle. It demands urgent pericardiocentesis.

Constrictive pericarditis

In constrictive pericarditis, the pericardium becomes rigid and fibrotic, adheres to the myocardium, and limits its function. It most commonly follows tuberculous pericarditis or hemopericardium, but can result from any cause of pericarditis.

The classic clinical picture is:

  • significant ascites
  • raised JVP with positive Kussmaul and Friedrich's signs
  • hepatomegaly
  • pulsus paradoxus (but usually less severe than in tamponade)
  • pericardial knock (high-pitched early diastolic added sound)
  • calcification visible on the lateral CXR

The most difficult differential diagnosis is restrictive cardiomyopathy. However, the left ventricular function is usually preserved in constrictive pericarditis, and filling pressures are raised. The only treatment for constrictive pericarditis is surgical excision of the pericardium.

Copyright © 2004, Remedica.
Bookshelf ID: NBK2211


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