The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. This procedure has significant risk involved, with mortality rates of 6% or higher in major referral centers.

A poor outcome is almost always the result after a pericardiectomy is performed for constrictive pericarditis whose origin was radiation-induced, further some patients may develop heart failure post-operatively.

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:

- subacute onset

- high fever (> 100.4 F/38 C) and leukocytosis

- development of cardiac tamponade

- large pericardial effusion (echo-free space > 20 mm) resistant to 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:

- 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. Depending on severity, dosing is between 300–800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours. 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.

Colchicine, which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies. 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. 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. It should be avoided or used with caution in patients with severe renal insufficiency, hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders.

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.

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). 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. The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart.

Dressler syndrome is best treated with high dose aspirin. In some resistant cases, corticosteroids can be used but are not preferred (avoided) in first month due to the high frequency of impaired ventricular healing leading to increased rate of ventricular rupture. NSAIDs though once used to treat Dressler syndrome, are less advocated and should be avoided in patients with ischemic heart disease. One NSAID in particular, indomethacin, can inhibit new collagen deposition thus impairing the healing process for the infarcted region. NSAIDS should only be used in cases refractory to aspirin. Heparin in Dressler syndrome should be avoided because it can lead to hemorrhage into the pericardial sac leading to tamponade. The only time heparin could be used with pericarditis is with coexisting acute MI in order to prevent further thrombus formation.

Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. Some teams have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury.

Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving. If the patient has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action.

Treatment depends on the underlying cause and the severity of the heart impairment. Pericardial effusion due to a viral infection usually goes away within a few weeks without the treatment. Some pericardial effusions remain small and never need treatment. If the pericardial effusion is due to a condition such as lupus, treatment with anti-inflammatory medications may help. If the effusion is compromising heart function and causing cardiac tamponade, it will need to be drained, most commonly by a needle inserted through the chest wall and into the pericardial space called pericardiocentesis. A drainage tube is often left in place for several days. In some cases, surgical drainage may be required by cutting through the pericardium creating a pericardial window.

The treatment in viral or idiopathic pericarditis is with aspirin, or non-steroidal anti-inflammatory drugs (NSAIDs such as ibuprofen). Colchicine may be added to the above as it decreases the risk of further episodes of pericarditis.

Severe cases may require one or more of the following:

- pericardiocentesis to treat pericardial effusion/tamponade

- antibiotics to treat tuberculosis or other bacterial causes.

- steroids are used in acute pericarditis but are not favored because they increase the chance of recurrent pericarditis.

- in rare cases, surgery

- in cases of constrictive pericarditis, pericardiectomy

Initial management in hospital is by pericardiocentesis. This involves the insertion of a needle through the skin and into the pericardium and aspirating fluid under ultrasound guidance preferably. This can be done laterally through the intercostal spaces, usually the fifth, or as a subxiphoid approach. A left parasternal approach begins 3 to 5 cm left of the sternum to avoid the left internal mammary artery, in the 5th intercostal space. Often, a cannula is left in place during resuscitation following initial drainage so that the procedure can be performed again if the need arises. If facilities are available, an emergency pericardial window may be performed instead, during which the pericardium is cut open to allow fluid to drain. Following stabilization of the patient, surgery is provided to seal the source of the bleed and mend the pericardium.

In people following heart surgery the nurses monitor the amount of chest tube drainage. If the drainage volume drops off, and the blood pressure goes down, this can suggest tamponade due to chest tube clogging. In that case, the patient is taken back to the operating room for an emergency reoperation.

If aggressive treatment is offered immediately and no complications arise (shock, AMI or arrhythmia, heart failure, aneurysm, carditis, embolism, or rupture), or they are dealt with quickly and fully contained, then adequate survival is still a distinct possibility.

The cause of constrictive pericarditis in the developing world are idiopathic in origin, though likely infectious in nature. In regions where tuberculosis is common, it is the cause in a large portion of cases.

Causes of constrictive pericarditis include:

- Tuberculosis

- Incomplete drainage of purulent pericarditis

- Fungal and parasitic infections

- Chronic pericarditis

- Postviral pericarditis

- Postsurgical

- Following MI, post-myocardial infarction

- In association with pulmonary asbestos

About 30% of people with viral pericarditis or pericarditis of an unknown cause have one or several recurrent episodes.

Pericardial effusion ("fluid around the heart") is an abnormal accumulation of fluid in the pericardial cavity. Because of the limited amount of space in the pericardial cavity, fluid accumulation leads to an increased intrapericardial pressure which can negatively affect heart function. A pericardial effusion with enough pressure to adversely affect heart function is called cardiac tamponade. Pericardial effusion usually results from a disturbed equilibrium between the production and re-absorption of pericardial fluid, or from a structural abnormality that allows fluid to enter the pericardial cavity.

Normal levels of pericardial fluid are from 15 to 50 mL.

Tuberculous pericarditis is a form of pericarditis.

Pericarditis caused by tuberculosis is difficult to diagnose, because definitive diagnosis requires culturing "Mycobacterium tuberculosis" from aspirated pericardial fluid or pericardial , which requires high technical skill and is often not diagnostic (the yield from culture is low even with optimum specimens). The Tygerberg scoring system helps the clinician to decide whether pericarditis is due to tuberculosis or whether it is due to another cause: night sweats (1 point), weight loss (1 point), fever (2 point), serum globulin > 40g/l (3 points), blood total leucocyte count <10 x 10/l (3 points); a total score of 6 or more is highly suggestive of tuberculous pericarditis. Pericardial fluid with an interferon-γ level greater than 50/ml is highly specific for tuberculous pericarditis.

There are no randomized trials which evaluate the length of anti-tuberculosis treatment required for tuberculous pericarditis. There is a small but not conclusive benefit for treatment with a schedule of steroids with anti-tuberculosis drugs. Open surgical drainage of fluid though effective in preventing cardiac tamponade was associated with more deaths.

Myopericarditis is a combination of both myocarditis and pericarditis appearing in a single individual, namely inflammation of both the pericardium and the heart muscle. It can involve the presence of fluid in the heart. Myopericarditis refers primarily to a pericarditis with lesser myocarditis, as opposed to a perimyocarditis, though the two terms are often used interchangeably. Both will be reflected on an ECG. Myo-pericarditis usually involves inflammation of the pericardium, or the sac covering the heart.

The ACAM2000 smallpox vaccine has been known to cause myopericarditis in some people.

Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). It consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion.

Dressler syndrome is also known as postmyocardial infarction syndrome and the term is sometimes used to refer to post-pericardiotomy pericarditis.

It was first characterized by William Dressler at Maimonides Medical Center in 1956.

It should not be confused with the Dressler's syndrome of haemoglobinuria named for Lucas Dressler, who characterized it in 1854.

A couple of medications are used to relieve pleurisy symptoms:

- Paracetamol (acetaminophen) or anti-inflammatory agents to control pain and decrease inflammation. Only indomethacin (brand name Indocin) has been studied with respect to relief of pleurisy.

- Codeine-based cough syrups to control the cough

There may be a role for the use of corticosteroids (for tuberculous pleurisy), tacrolimus (Prograf) and methotrexate (Trexall, Rheumatrex) in the treatment of pleurisy. Further studies are needed.

Treatment has several goals:

- Relief of symptoms

- Removal of the fluid, air, or blood from the pleural space

- Treatment of the underlying condition

Uremic pericarditis is a form of pericarditis. It causes fibrinous pericarditis. The main cause of the disease is poorly understood.

Studies have shown no benefit for the use of herbal medicine on all cause mortality in viral myocarditis.

Uremic pericarditis is correlated to the degree of azotemia in the system. BUN is normally >60 mg/dL (normal is 7–20 mg/dL). The pathogenesis is poorly understood.

People who do not respond to conventional therapy are candidates for bridge therapy with left ventricular assist devices. Heart transplantation is reserved for people who fail to improve with conventional therapy.

Extracorporeal membrane oxygenation may be used in those who are about to go into cardiac arrest.

A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body.

While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.

Carditis is the inflammation of the heart or its surroundings. The plural of carditis is carditides.

It is usually studied and treated by specifying it as:

- Pericarditis is the inflammation of the pericardium

- Myocarditis is the inflammation of the heart muscle

- Endocarditis is the inflammation of the endocardium

- Pancarditis is the inflammation of the entire heart: the epicardium, the myocardium and the endocardium

- Reflux carditis refers to a possible outcome of esophageal reflux (also known as GERD), and involves inflammation of the esophagus/stomach mucosa

Until recently, it was generally assumed that the prognosis for individuals with diastolic dysfunction and associated intermittent pulmonary edema was better than those with systolic dysfunction. In fact, in two studies appearing in the New England Journal of Medicine in 2006, evidence was presented to suggest that the prognosis in diastolic dysfunction is the same as that in systolic dysfunction.

Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

Treatment of restrictive cardiomyopathy should focus on management of causative conditions (for example, using corticosteroids if the cause is sarcoidosis), and slowing the progression of cardiomyopathy. Salt-restriction, diuretics, angiotensin-converting enzyme inhibitors, and anticoagulation may be indicated for managing restrictive cardiomyopathy.

Calcium channel blockers are generally contraindicated due to their negative inotropic effect, particularly in cardiomyopathy caused by amyloidosis. Digoxin, calcium channel blocking drugs and beta-adrenergic blocking agents provide little benefit, except in the subgroup of restrictive cardiomyopathy with atrial fibrillation. Vasodilators are also typically ineffective because systolic function is usually preserved in cases of RCM.

Heart failure resulting from restrictive cardiomyopathy will usually eventually have to be treated by cardiac transplantation or left ventricular assist device.