Acute pericarditis

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Acute pericarditis
An ECG showing pericarditis. Note the ST elevation in multiple leads with slight reciprocal ST depression in aVR.
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Acute pericarditis is a type of pericarditis (inflammation of the sac surrounding the heart, the pericardium) usually lasting less than 6 weeks.[citation needed] It is the most common condition affecting the pericardium.

Signs and symptoms

GERD, pulmonary embolism
, muscular pain, etc.

A

systole, ventricular systole, and the filling phase of early ventricular diastole
.

Fever may be present since this is an inflammatory process.

Causes

There are several causes of acute pericarditis.

Familial mediterranean fever and TNF receptor associated periodic syndrome are rare inherited autoimmune diseases capable of causing recurring episodes of acute pericarditis.[1]

Pathophysiology

Clinical presentation of diseases of pericardium may vary between:[2][3]

Diagnosis

ECG showing slight ST elevation in many leads congruent with pericarditis

For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a

electrocardiogram (ECG) consistent with acute pericarditis.[1]

A

Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis.[7]

epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes[4][8]

The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization.[9] As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities.[10] In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia.[11]

Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign.[12] It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick's sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodick's sign is often a giveaway to the diagnosis.[citation needed]

Rarely, electrical alternans may be seen, depending on the size of the effusion.[citation needed]

A chest x-ray is usually normal in acute pericarditis but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.[citation needed]

An

echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.[citation needed
]

Treatment

Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include the following:[13]

  • subacute onset
  • high fever (> 100.4 F/38 C) and leukocytosis
  • development of cardiac tamponade
  • large
    NSAID
    treatment
  • immunocompromised
  • history of oral anticoagulation therapy
  • acute trauma
  • failure to respond to seven days of NSAID treatment

Pericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions:[14]

  • presence of moderate or severe cardiac tamponade
  • diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis
  • persistent symptomatic pericardial effusion

NSAIDs in viral or idiopathic pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range.[14] Depending on severity, dosing is between 300 and 800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours.[13] Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.[citation needed
]

Colchicine, which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies.[15] Colchicine can be given 0.6 mg twice a day (0.6 mg daily for patients <70 kg) for 3 months following an acute attack. It should be considered in all patients with acute pericarditis, preferably in combination with a short-course of NSAIDs.[9] For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or twice daily for three months.[16][17][18][19][20] It should be avoided or used with caution in patients with severe chronic kidney disease, hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders.[9]

Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease.[16]

Prognosis

One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. Signs of cardiac tamponade include distended neck veins, muffled heart sounds when listening with a stethoscope, and low blood pressure (together known as Beck's triad).[1] This condition can be fatal if not immediately treated.

Another longer term complication of pericarditis, if it recurs over a longer period of time (normally more than 3 months), is progression to constrictive pericarditis. Recent studies have shown this to be an uncommon complication.[21] The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart.[citation needed]

References

  1. ^
    PMID 25517707
    .
  2. S2CID 25862792
    .
  3. PMID 20511488
    .
  4. ^
    PMID 12622586
    .
  5. PMID 10781355
    .
  6. ^
    PMID 14680742
    .
  7. ISBN 978-1-4051-4166-6
    .
  8. S2CID 208789653
    .
  9. ^
    ISBN 978-1842145432
    .
  10. S2CID 5389517
    .
  11. PMID 22516141
    .
  12. PMID 24626086
    .
  13. ^
    PMID 15028364
    .
  14. ^
    PMID 15120056
    .
  15. PMID 25404591
    . Retrieved 2015-12-22.
  16. ^
    PMID 24190942
    .
  17. S2CID 207381123
    .
  18. PMID 8184826
    .
  19. PMID 16186437
    .
  20. PMID 16186468
    .
  21. S2CID 32460894
    .

Further reading

External links

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