Pericarditis
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Introduction 

Pericarditis is a common cause of chest pain, and may mimic the signs and symptoms of myocardial infarction. It is a result of inflammation of the pericardium. 

The two most common causes of pericarditis are viral infection and secondary to myocardial infarction, although normally when people talk about pericarditis, they are referring to the viral variety.

It is characterised by central or left sided chest pain, that is worse on inspiration, or lying down and relieved by sitting forwards. In severe cases, cardiac tamponade (compression of the heart) can result, which may also cause shortness of breath.

The classical ECG findings are saddle shaped ST elevation and PR depression – both of which are often widespread in many leads (unlike the location specific pattern of ST elevated seen in myocardial infarction).

Most cases are mild, and it typically resolves within a few weeks. Treatment is often with NSAIDs or colchicine.

  • Occasionally chronic pericarditis can occur, with long-stand and slowly progressive accumulation of fluid in the pericardium
  • It is typically secondary to an acute viral pericarditis

The normal pericardium

The pericardium is the fluid-filled sac that surround the heart. The normal pericardium contains about 50ml of fluid, and helps lubricate the movement of the heart. It also:
  • Limits distension of the heart
  • Protects the heart from infection / damage
  • Aids the filling of the ventricles
Congenital defects of the pericardium do not appear to have much impact on heart function.

Acute Pericarditis

Causes

  • Infection (most commonly viral, but often not identified). The most common causatory factors are coxsackie B virus, influenza, adenovirus and echovirus.
  • Acute MI – post MI pericarditis occurs in about 20% of MI patients. It occurs most commonly with anterior MI’s and MI’s with massive ST elevation.
  • The incidence is actually reduced by 5-6% with thrombolysis
  • It can be difficult to differentiate this pain from angina pain within the first couple of days after an MI
  • Dressler’s syndrome is pericarditis that occurs secondary to myocardial or pericardial damage, and occurs at least 2 weeks after the MI. this makes it different from the normal post MI pericarditis described above. Dressler’s occurs in about 7% of MI patients.The symptoms can arise anywhere between a few weeks and 2 years after an MI, and will usually subside within a few days. Typical time of onset is 1 to 4 weeks after the MI.
    • It is an auto-immune condition whereby the body auto-reacts against damaged myocardial tissue. Antimyocardial antibodies are often found.
    • Recurrence is common
    • May also occur after episodes of unstable angina
    • Presents with massively raised ESR

Less common causes

  • Autoimmune reaction
  • Trauma
  • Neoplasm
  • Idiopathic
  • Bacterial infection
  • TB
  • Rheumatic fever
  • HIV – these patient may get staphylococcal pericarditis – which is often fatal

Pericarditis and myocarditis often co-exist

Signs and Symptoms

Sharp pain – this can vary in site and severity, however is usually retrosternal. It often radiates to the shoulders and neck, and is aggravated by deep breathing (pleuritic), movement, change of position, exercise and swallowing.

  • The pain is typically relieved by leaning forwards, and worse when lying flat
  • The main differentials for this type of pain are pleurisy and pericarditis

Fever – a low grade fever may be present
Pericardial effusion – this is present whatever the cause. However, it can be a result of different factors (depending on the cause); e.g. serous, purulent, haemorrhagic, fibrinous

  • Fibrinous exudatescan eventually lead to adhesion
  • Serous – this produces a large amount of straw-coloured fluid, with a very high protein content
  • Haemorrhagic – usually due to malignant disease, most commonly carcinoma of the breast, bronchus, and lymphoma.
  • Purulent – this is rare, and may be a complication of septicaemia.
  • Pericardial effusion may press on the surrounding tissues, particularly the bronchi, resulting in dyspnoea

Pericardial friction rub – this is a high pitched superficial scratching or crunching sound, that is produced by movement of the pericardium. It is diagnostic for pericarditis. Usually heard in systole but may also be heard in diastole.

  • It is classically heard in three, or two (‘to and fro’ rub) phases – i.e. this means it is heard 3 times or twice during one cardiac cycle
  • The rubs are typically heard best with the diaphragm at the left lower sternal edge at full expiration

Investigations

There is no specific diagnostic test. Diagnoses should be based on clinical history – e.g. recent viral infection (+/- absence of risk factors for cardiovascular disease), a suggestive ECG, and other supportive information – such as raised WCC or inflammatory markers.

It is important to exclude other more serious causes of similar chest pain such as myocardial infarction, myocarditis and pulmonary embolus.

ECGthis will show widespread saddle shaped ST elevation. There may also be PR interval depression – and if both of these are present it is diagnostic of pericarditis

  • Later there may also be T wave inversion – especially if myocarditis is also present. This will eventually resolve
  • The ST elevation is often distributed in both inferior and anterior leads – thus this helps to distinguish it from MI
Pericarditis ECG
Pericarditis ECG. Note thePR depression – particularly in leads I, II and V2-V6, as well as the dalle shaped ST elevation – most prominent in I, II and V4-V6. This file is taken from wikimedia commons and is licensed under the Creative Commons Attribution-Share Alike 3.0 Unported license.
  • FBC – there may be leukocytosis or lymphocytosis due to viral or bacterial infection
  • CRP / ESR – may be raised and if so, help to support the diagnosis
  • CXR, echo, radionucleotide scans – these are all of little use in uncomplicated disease

Treatment

Be wary to properly identify the underlying cause!

If confident of a simple viral pericarditis:

  • Colchicine
    • 500mcg BD for 3 months
      • OD if weight <70kgs
  • PLUS
  • Oral NSAID’s
    • Ibuprofen 600mg TDS for two weeks, then 200-400mg TDS for 2 weeks, OR
    • Aspirin 750-1000mg TDS  for 2 weeks and then 250-500mg TDS for 2 weeks
    • Do not use NSAID’s in the first few days after MI – as they associated with increased risk of myocardial rupture
Most cases resolve within a few weeks without complication.

Complications

  • If pericarditis lasts more than 6-12 months, then chronic pericarditis is said to exist. In these cases, it is possible for the pericardium to thicken, and this can restrict ventricular filling, and then restrictive pericarditis is present

Pericardial effusion and cardiac tamponade

Pericardial effusion – this is collection of fluid within the pericardial sac. It most commonly occurs with pericarditis. When the pericardial sac fills, this puts pressure on the ventricles, and compromises their pumping function. This causes problems with circulation. When this occurs, it is known as cardiac tamponade. Tamponade generally comes on very quickly – it is acute heart failure due to compression.

Clinical features

  • Heart sounds soft and distant
  • Apex beat is commonly obscured
  • Friction rub – may be present in the early stages (of pericarditis), but as the amount of fluid increases, the rub disappears
  • Ewart’s sign – this is rare – the effusion can compress the base of the left lung producing an area that is dull to percussion, just below the angle of the left scapula.
  • Features of tamponade
  • Raised JVP, with a sharp rise, and sharp y descent  – Freidrich’s sign.
  • Kussmaul’s sign – raised JVP + increased neck vein distension in inspiration
  • Pulsus paradoxus – this is an exaggeration of the normal variation of the pulse during inspiration and expiration. Normally the pulse is stronger during inspiration, and weaker during expiration. This becomes exaggerated such that the radial pulse may not be palpable, due to a substantial drop in BP

Investigations

  • ECG – low voltage QRS complexes
  • CXR – will show an enlarged heart (globular or pear shaped), with precise outlines. The pulmonary veins will not be distended.
  • Echo – this is the most useful test, as it is able to directly detect the tamponade
  • MRI – maybe do one of these if you suspect haemopericardium
  • Pericardiocentesis – this is indicated when you suspect an infection is the cause (e.g. TB, malignancy)
  • Pericardial biopsy – this can be done if you still suspect TB, despite a negative pericardiocentesis
  • Blood cultures / antibody screen – to look for the underlying cause

Treatment

Treat the underlying cause – most pericardial effusions resolve spontaneously.
In cases of a rapid forming effusion, then tamponade will probably result; and acute treatment would involve pericardiocentesis, and perhaps a drain, just to allow the fluid to escape.
  • If it keeps coming back after being drained, then it is most likely the result of malignancy. If this is the case, then you can treat it with fenestration – which is where you create a ‘window’ in the pericardium, which allows the fluid to drain into the surrounding tissue

Constrictive pericarditis

This can be a result of TB and other infectious causes. The pericardium may become hard, fibrous and calcified. It also occurs after open heart surgery. Most of the time it is asymptomatic, but if it starts to interfere with ventricular filling, then we say constrictive pericarditis is present.
  • Generally, the changes occur over a long period of time, and thus other mechanisms have time to compensate. Thus it is not as dangerous as tamponade.
The signs and investigations are very similar to that of pericardial effusion. However, there may be other more chronic signs also, such as:
  • Pulmonary effusion – dyspnoea, cough, orthopnoea
  • Reduced cardiac output – hypotension, fatigue, reflex tachycardia
  • Pulmonary venous congestion – ascites, hepatomegaly, raised JVP
  • Atrial dilation – which in 30% of patients will cause atrial fibrillation
  • Constrictive pericarditis is very difficult to distinguish from restrictive cardiomyopathy. The final diagnosis may depend on complex Doppler flow studies.

Treatment

This involves complete resection of the pericardium. This is dangerous, and has a high rate of complications. the earlier in the progression of the disease that the resection is performed, the greater the chance of success.
If TB is also present, then the calcified pericardium suggests chronic disease.

References

  • Pericarditis - eTG
  • Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
  • Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
  • Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) currently works as a GP Registrar and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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