The normal pericardium
- Limit distension of the heart
- Protect the heart from infection / damage
- Aids the filling of the ventricles
Infection (most commonly viral, but often not identified). The most common causatory factors are coxsackie B virus 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
- Bacterial infection
- 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
- The differentials for this type of pain are basically 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 exudates – can 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
- 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
- Treat the underlying cause!
- Bed-rest and oral NSAID’s. however – do not use NSAID’s in the first few days after MI – as they associated with increased risk of myocardial rupture.
- Corticosteroids may be given as symptomatic relief, but there is no evidence that they increase the speed of cure
- 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
- 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
- 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
- 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
- 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.
- 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.