Pericarditis

a chest x-ray will detect pulmonary congestion and heart size, while a Doppler ultrasound will evaluate the pressures inside the heart.

Most of the time, mild valvular disorders can be managed symptomatically until it becomes necessary to replace or repair the valve. A valvuloplasty is a valve repair surgery, while valve replacement can involve an artificial valve or a porcine, pig-derived or bovine, cow-derived valves. Those with valvular disease often require antibiotic prophylaxis to prevent bacterial vegetations from developing during certain surgical or dental procedures.

Patients with a prosthetic valve will require long-term anticoagulation therapy, especially if the person has a mechanical valve. The target IRN should be quite high in order to avoid thromboemboli from occurring. The only accepted anticoagulant for those who have prosthetic valves is warfarin. The newer anticoagulants are insufficient, although heparin can be used if warfarin is not recommended, such as with a pregnant patient. Patients who also have stents will require aspirin, clopidogrel, and warfarin at the same time.

PERICARDITIS

Pericarditis represents an inflammation of the pericardium, usually with accumulation of fluid in the pericardial sac. The inflammation can be due to infection, trauma, myocardial infarction, cancer, or metabolic disease. The patient will have pain or tightness in their chest, worse with deep inspiration. If there is constriction or decreased cardiac output associated with this, there will be symptoms of cardiac tamponade.

Remember that the pericardium has two layers: the visceral layer attached to the myocardium and the parietal layer covering the heart. The pericardial sac contains a very small amount of fluid under normal circumstances. These layers are stretchsensitive so it doesn’t take much extra fluid to cause increased pain.

Pericarditis may be acute, subacute, or chronic. Acute pericarditis develops quickly and often leads to a pericardial effusion and secondary inflammation of the outer myocardial layers. Subacute pericarditis comes on within weeks to months and can be an extension of acute disease. Chronic pericarditis happens after six months of inflammation. The

fluid that builds up can be chyle, pus, blood, serous, or serosanguineous in nature. If cardiac tamponade happens, the cardiac output will drop and fluid backs up, and shock can occur. Symptoms will be less if the fluid buildup happens slowly versus when it comes more quickly.

Constrictive pericarditis is not common but comes when the pericardium is fibrotic and thick. Calcium deposits and scar tissue between the layers can complicate the picture. It is more common for these to lead to rhythm disturbances than to fluid accumulation. The problem is that the cardiac output drops so much that there will be an elevation of venous pressures, hepatic congestion, and cirrhosis from this congestion.

Most cases of acute pericarditis are inflammatory from radiation, drugs, uremia, myocardial infarction, infection, or autoimmune disease. Most infectious cases are viral or cannot be identified at all. Post-MI pericarditis is called Dressler syndrome, which is now less commonly seen.

Chronic pericarditis can also have the same etiologies as acute and subacute pericarditis, although cholesterol pericarditis and hypothyroidism can also be causative of the symptoms. Another common cause of chronic pericarditis is some type of metastatic cancer.

Most acute pericarditis patients will have significant pain and an obvious pericardial friction rub. Some will be short of breath. If there is tamponade, you can expect hypotension, pulmonary edema, jugular venous distension, and other evidence of venous congestion. The pain may be similar to an MI because of the similarities in their innervation but inspiration and swallowing may exacerbate the symptoms. If the cause is inflammatory or infection, the patient may have fever, chills, and cough.

Chronic pericarditis and constrictive pericarditis do not always have the same symptoms but, if the cardiac output is impaired, the major finding will be of peripheral venous congestion, such as hepatomegaly, jugular venous distension, and peripheral edema. An echocardiogram and ECG plus a chest x-ray will help identify a pericardial effusion but won’t identify tamponade because large volumes of up to 1500 milliliters of fluid will be tolerated if the buildup is gradual. Cardiac tamponade is a clinical and not an imaging diagnosis.