Pericarditis means inflammation of the pericardium, the two-layered sac that surrounds the heart and the first part of the great vessels. It is a common cause of acute chest pain: roughly 5% of patients who reach an emergency department with chest pain that turns out not to be a myocardial infarction have it. The diagnosis is made from the history, the physical examination and the electrocardiogram (ECG).
The pericardium and what it does
The pericardium is a fibro-serous sac. Its inner visceral layer, also called the epicardium, is a thin sheet of mesothelial cells closely adherent to the surface of the heart. This layer is reflected onto the outer fibrous layer and together they form the parietal pericardium, built from collagenous fibrous tissue and elastic fibrils. Between the two layers sits the pericardial space, holding about 10–50 mL of fluid — an ultrafiltrate of plasma — drained by the right lymphatic duct and the thoracic duct.
Four functions are usually listed for this sac. It stabilises the heart within the chest through its ligamentous attachments, limiting how far the heart can move. It protects the heart from mechanical trauma and from infection spreading from adjacent structures. Its fluid lubricates the cardiac surface, reducing friction during systole and diastole. And it resists excessive dilation of the heart when intracardiac volume rises suddenly, as in acute aortic or mitral regurgitation.
That last function is also why the pericardium causes trouble when fluid collects inside it: a sac stiff enough to resist sudden dilation is a sac that transmits pressure to the chambers it encloses. Because the sac cannot stretch quickly, the rate at which fluid arrives — rather than the total volume — decides whether the heart becomes compressed, which is the mechanism behind cardiac tamponade.
Causes
Pericarditis has a long list of causes, usually grouped into seven categories. They differ in how common they are and in whether finding them changes treatment, a point taken up after the list.
- Infective. Viral causes predominate — coxsackieviruses A and B, influenza, adenovirus and HIV are the classic names, and parvovirus B19 and herpesviruses such as Epstein–Barr virus and cytomegalovirus are also described. Bacterial pericarditis involves Staphylococcus, pneumococcus or Mycobacterium tuberculosis. Fungal causes include Candida species, and parasitic causes are recognised though uncommon.
- Autoimmune disorders. Systemic lupus erythematosus (SLE), drug-induced lupus from agents such as hydralazine or procainamide, rheumatoid arthritis, and the post-cardiac-injury syndromes (pericardial inflammation that follows damage to the heart), including Dressler syndrome after myocardial infarction.
- Neoplasm. Primary mesothelioma, a tumour arising from the mesothelial cells that line the pericardium, is rare. Secondary metastatic involvement and direct extension from an adjoining tumour are more common.
- Radiation pericarditis, typically after mediastinal radiotherapy.
- Renal failure (uraemia), the build-up of waste products in the blood, in end-stage renal disease.
- Traumatic cardiac injury, both penetrating (stab and gunshot wounds) and blunt (for example a steering-wheel injury).
- Idiopathic — no cause identified despite investigation.
How these categories are distributed depends heavily on where the patient is and how hard the clinician looks. In developed countries, idiopathic and presumed-viral cases make up the large majority, with reported proportions between roughly 50% and 90% depending on the case mix and the extent of the workup; a specific non-viral cause is found in a minority. Tuberculous pericarditis remains an important cause in regions where tuberculosis is common, and it is one of the causes where identifying the organism changes treatment rather than only explaining the symptoms.
The clinical picture
Whatever the cause, the diagnosis begins at the bedside, with the pain and how it behaves.
The classic triad of acute pericarditis is pleuritic chest pain (pain that is worse with breathing), fever and a pericardial friction rub, a scratching sound made by the inflamed layers. Chest pain is by far the most consistent element, present in about 85–90% of cases. It is characteristically sharp, worse on inspiration, coughing and lying flat, and eased by sitting up and leaning forward. The positional quality has a simple explanation: the inflamed visceral and parietal layers rub against each other as the heart moves inside the chest, and changing posture changes how much they touch.
The pericardial friction rub is the most specific physical finding, but it is present in only about a third of patients or fewer, and it comes and goes. Listening repeatedly is worthwhile. It has three components, best heard with the diaphragm of the stethoscope at the left lower sternal border: an atrial or pre-systolic component, a ventricular systolic component — the loudest of the three — and a ventricular diastolic component.
Low-grade fever and a sinus tachycardia (a fast heart rate with a normal sinus rhythm) are common. A temperature above 38 °C is not, and when it is present it points towards a severe inflammatory episode or to purulent bacterial pericarditis. One question is worth asking of every patient with chest pain and a suspected pericardial cause: whether they had fever or an upper airway infection in the previous month, since that recent viral prodrome is a frequent clue.
Other causes of the same chest pain
The differential is, in practice, every other cause of chest pain: acute coronary syndrome, pulmonary embolism, aortic dissection, pneumonia, pleuritis, costochondritis and gastro-oesophageal reflux. Four features push the balance towards pericarditis — pain that changes with posture and breathing, a friction rub, a diffuse ECG pattern without reciprocal ST depression (the mirror-image lowering of the ST segment that accompanies infarction), and a recent viral illness. Myocarditis, inflammation of the heart muscle, overlaps substantially, because the same viruses inflame the myocardium next door, and around 15% of episodes of pericarditis have a measurable myocardial component with a rise in troponin, a protein released by injured heart muscle.
Because infarction is the most dangerous item on that list, the ECG becomes the next step in telling it apart from pericarditis.