Pericarditis

A patient tells you they have a sharp pain in the centre of their chest. It becomes worse when they take a deep breath or lie flat, but sitting forward seems to ease it. That pattern fits pericarditis quite well, although chest pain still needs to be assessed properly because myocardial infarction, pulmonary embolism and other important causes can present alongside some of the same features.

To understand the pain, it helps to picture where the inflammation is. The heart sits inside the pericardium, a sac made up of an outer fibrous layer and inner serous layers. Between the serous layers is a small amount of fluid, allowing the heart to move with very little friction as it fills and contracts. In pericarditis, those normally smooth surfaces become inflamed.

What does an inflamed pericardium feel like?

Every heartbeat moves the heart within the pericardial sac, and breathing changes the position of the heart and surrounding structures. When the pericardium is inflamed, that movement can become painful. This is why the pain is often pleuritic, becoming sharper with inspiration, and why changing position can alter it. Sitting forward may reduce the discomfort, while lying flat can make it worse.

Sometimes the inflamed pericardial surfaces can be heard rubbing against one another. A pericardial friction rub has a scratchy or grating quality and can come and go, so not hearing one does not rule pericarditis out.

The cause is not always identified. Pericarditis may follow a viral illness, but it can also occur after myocardial injury or cardiac surgery and alongside autoimmune disease, kidney failure, malignancy, tuberculosis or bacterial infection. The history therefore reaches beyond the chest pain itself. Recent infection, cardiac procedures, other illnesses and medicines can all help the clinical team decide whether this is likely to be uncomplicated acute pericarditis or whether another cause needs investigating.

The inflammation does not always stop at the pericardium

The pericardium lies directly against the myocardium, and sometimes inflammation involves both. If myocardial cells are injured, troponin can rise. That can make the initial picture more complicated because chest pain, ECG changes and a raised troponin are also findings that immediately raise concern about an acute coronary syndrome.

A raised troponin in somebody with suspected pericarditis therefore needs context. It tells you that myocardial injury has occurred, not what caused it. When myocardial involvement is more substantial, ventricular function and cardiac rhythm can also be affected.

What might you see on the ECG?

Pericardial inflammation can affect the electrical appearance across a broad area of the heart. The classic teaching pattern is widespread ST-segment elevation with PR-segment depression. That is different from the more territorial changes often associated with an acute coronary occlusion, but real patients do not always arrive with textbook ECGs.

Some people with acute pericarditis have no typical ECG changes at all. The ECG therefore sits alongside the history, examination, inflammatory markers, cardiac biomarkers and imaging rather than making the diagnosis by itself.

Echocardiography gives the team another piece of the picture. It can show whether fluid has collected around the heart and whether cardiac function is being affected. Cardiac magnetic resonance imaging can show pericardial and myocardial inflammation and can be particularly useful when the diagnosis remains uncertain or myocardial involvement is suspected.

Bleepbook's 12-Lead ECG Explained looks separately at how the different leads view cardiac electrical activity.

What changes when fluid begins to collect?

Inflammation can cause fluid to accumulate between the pericardial layers. This is a pericardial effusion. An effusion is not the same thing as cardiac tamponade, and the difference becomes much easier to understand if you think about the heart trying to fill inside a sac with increasingly less room available.

If fluid accumulates slowly, the pericardium has time to stretch. A patient may therefore tolerate quite a large chronic effusion without the circulation collapsing. If fluid accumulates quickly, the pericardium has much less time to adapt. Even a smaller volume can raise pressure around the heart enough to interfere with filling.

Venous blood is still returning to the heart, but rising pressure inside the pericardial space begins to oppose the pressure filling the cardiac chambers. The right atrium and right ventricle are particularly vulnerable because their filling pressures are relatively low. As those chambers become harder to fill, less blood moves through the heart and ventricular stroke volume falls.

The body initially tries to compensate. The heart rate may increase to help maintain cardiac output. But if filling continues to deteriorate, compensation may no longer be enough. Once pressure from the pericardial fluid is restricting cardiac filling and compromising the circulation, the patient has cardiac tamponade.

This is where the bedside picture can change. A patient who initially had positional chest pain may become increasingly breathless and tachycardic. Blood pressure may fall. Jugular venous pressure may rise because venous blood is struggling to enter the compressed right side of the heart. As cardiac output falls, the patient may develop cool peripheries, reduced urine output or altered cognition.

Beck's triad describes hypotension, muffled heart sounds and raised jugular venous pressure, but waiting for all three would be unsafe because the complete triad is not present in every patient. Echocardiography can show the effusion and whether it is interfering with chamber filling. Haemodynamic compromise may require urgent drainage of the pericardial fluid.

Settling the inflammation and watching the patient recover

For uncomplicated acute pericarditis, treatment usually focuses on controlling the inflammation and reducing recurrence. Current European Society of Cardiology guidance recommends aspirin or a non-steroidal anti-inflammatory drug, with colchicine when appropriate. The anti-inflammatory medicine helps relieve pain and inflammation, while colchicine reduces the likelihood of another episode.

The prescription still has to fit the person in front of you. Renal function, gastrointestinal risk, anticoagulant treatment, pregnancy and other medicines can affect which treatments are suitable. Corticosteroids are not routinely the first choice for uncomplicated idiopathic pericarditis, although there are situations where they are appropriate. Recurrent disease or a specific underlying cause may need a different specialist approach.

As the pain settles, assessment does not simply stop. Recovery may also be followed through symptoms, inflammatory markers, ECG findings and imaging, particularly when there has been an effusion or myocardial involvement. Physical activity is restricted while active inflammation is present, with return to activity guided by clinical recovery and the extent of cardiac involvement.

For the patient, one of the most useful explanations is the connection between their symptoms and the anatomy. The pain comes from inflammation around a moving heart. An effusion means fluid has collected within that same confined space. If the pressure becomes high enough to stop the chambers filling properly, the problem changes from painful inflammation to a threat to the circulation. Following that sequence makes the observations at the bedside much easier to interpret.

References

European Society of Cardiology (2025) 2025 ESC Guidelines for the management of myocarditis and pericarditis.

European Society of Cardiology (2025) Pocket Guidelines on Myocarditis and Pericarditis.

British Heart Foundation Pericarditis.

Adler, Y. et al. (2015) 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. European Heart Journal, 36(42), pp. 2921–2964.

Imazio, M. et al. (2013) A randomized trial of colchicine for acute pericarditis. New England Journal of Medicine, 369, pp. 1522–1528.