Symptoms include; flu-like illness with chest pain when the pericardium is involved, arrhythmias, or signs of right- and left-sided congestive heart failure. Patients with myocarditis oftentimes present with signs and symptoms of acute decompensation of heart failure e. Left ventricular dilatation can lead to expansion of the mitral valve ring and a mitral regurgitant murmur. A S3 gallop indicates left-sided congestive heart failure.
Viruses directly invade the myocytes and cause damage to the infected cells. The immune response to infection also causes damage to the myocytes.
Immune cell infiltration of the myocytes includes T-lymphocytes predominantly accompanied by macrophages and B-lymphocytes. Circulating autoantibodies directed against mitochondria and contractile proteins are frequently detected and may cause further damage. Cytokines and oxygen free radicals have also been implicated in causing damage to the myocytes. Diagnosis of myocarditis involves identifying the signs and symptoms of cardiac failure.
A peripheral blood complete blood count usually reveals a leukocytosis. They usually have an elevated erythrocyte sedimentation rate and increased levels of acute phase proteins in their blood stream e.
Chest radiographs can be used to detect pulmonary edema in congestive heart failure and cardiac dilatation. Echocardiography can be used to assess cardiac contractility, chamber size, valve function, and wall thickness and to exclude other causes of heart failure e. Contrast-enhanced MRI can detect the extent and degree of inflammation and determines parameters that correlate with left ventricular function and clinical status.
To obtain a definitive diagnosis an endomyocardial biopsy is needed however this is not usually done. Most cases of viral myocarditis are self-limited and are followed by full recovery. Viral myocarditis is usually a mild disease and responds well to bed rest. Cardiac monitoring may be required to alert caregivers to potentially life-threatening arrhythmias.
Glucosteroids and other immunosuppressive drugs are contraindicated. Endocarditis is an inflammation of the endothelium that lines the inside of the heart. Certain areas of the endothelium are more likely to be affected in endocarditis and they include the surfaces of the heart valves. Some heart valves are more commonly affected than others. The etiology of endocarditis depends on the condition of the heart valve, if the person is an intravenous drug user, if the patient has a prosthetic heart valve, and how long the prosthetic heart valve has been in place See Table E Table E Streptococcus i.
Gram-negative bacilli, HACEK group Haemophilus aphrophilus Haemophilus parainfluenzae or Haemophilus paraphrophilus , Actinobacillus actinomycetemcomitans , Cardiobacterium hominis , Eikenella corrodens , Kingella kingae , Coxiella burnetii , and Chlamydia.
Staphylococcus Staphylococcus aureus and Staphylococcus epidermidis , gram-negative aerobic bacilli. Late more than 2 months post heart surgery. Viridans Streptococcus , Staphylococcus epidermidis , and Staphylococcus aureus. Staphylococcus aureus and gram-negative bacilli Pseudomonas aeruginosa is most the common gram-negative bacilli. Viridans Streptococcus, Enterococcus, Candida albicans , polymicrobial infections. Two types of infectious endocarditis occur: subacute and acute.
Subacute endocarditis is more common and takes more time for symptoms to develop. Oftentimes the symptoms are nonspecific. Acute endocarditis progresses very rapidly with more severe symptoms.
Acute endocarditis is more common in intravenous drug users and in staphylococcal infections of the heart. In subacute endocarditis the interval between the colonization of the endocardium and the onset of symptoms is usually less than two weeks. Because the symptoms are usually nonspecific, on average there is a delay of five weeks between onset of symptoms and diagnosis.
The most common symptom is a low-grade fever range of 38oC. Only in acute endocarditis does the temperature go above 40oC. Fever is usually accompanied by chills and sometimes by night sweats. Fatigue, anorexia, weakness, myalgias, arthralgias and malaise are common. Debilitating low back pain is a prominent complaint in a small percentage of patients. Acute endocarditis has a rapid onset e.
Acute endocarditis is usually caused by Staphylococcus aureus or Enterococcus. The patient usually has a high fever is high 40oC and rigors. Patients are very ill appearing. The likelihood of extravascular complications is higher.
The following signs and symptoms can be seen in patients with subacute or acute endocarditis. Nearly all patients will have an audible heart murmur.
Although classically described as a changing murmur the murmur usually does not change significantly over time unless a valve leaflet is destroyed or a chordae tendineae ruptures. Murmurs are less common in right-sided endocarditis. Roth spots or flame-shaped hemorrhages may be observed on funduscopic examination. Roth spots are retinal hemorrhages with pale centers. Petechial hemorrhages can occur in the conjunctiva, the buccal mucosa, palate, extremities, and splinter hemorrhages under the nail beds of the hands and feet.
Janeway lesions are painless hemorrhagic plaques on the palms and soles. Osler nodes are small, pea-sized subcutaneous, painful erythematous nodules that occur in the pads of the fingers and toes and the thenar eminence. They are usually present for a brief period of time lasting only a few hours to a couple of days. Complications occur in most patients and include cardiac complications e.
Infective endocarditis is usually preceded by the formation of a predisposing cardiac lesion. Endothelial cells that line the inside of the heart and the heart valve can become damaged leading to the accumulation of platelets and fibrin producing a nonbacterial thrombotic endocarditis NBTE. This sterile lesion serves as an ideal site for bacteria to attach to when in the bloodstream.
Various conditions lead to endothelial cell damage and predispose a patient to the formation of NBTE. They include: rheumatic heart disease, congenital heart disease i. Intravenous drug users are at higher risk of developing endocarditis due to their propensity to inject bacterially contaminated solutions intravenously.
Patient recovering from endocarditis are also at increased risk of having a second episode of endocarditis. Shear stress can also damage the surface of the valves. The valves that get the most shear stress are the ones on the left side of the heart i. With the exception of intravenous drug users right-sided endocarditis is uncommon. When right-sided endocarditis does occur it is usually on the tricuspid valve.
Microorganisms growing in the normal flora of the body cause most cases of infective endocarditis. They gain access to the blood intermittently, as a result of minor trauma to the mucosa of the oropharynx, gastrointestinal tract, or genitourinary tract.
Such transient bacteremias usually occur without ill effects but they may lead to endocarditis in patients with an underlying NBTE or artificial heart valve. Bacteria and platelets tend to accumulate on the downstream or low-pressure side of a valvular NBTE.
When bacteria colonize the NBTE they form vegetations. Surface adherence factors are essential for the bacteria to colonize the NBTE e. Staphylococcus aureus binds to fibronectin. The bulk of the vegetation is an amorphous mass of fibrin and platelets containing colonies of microorganisms. These vegetations vary in size from tiny bodies to masses large enough to occlude valve orifices.
Abscesses may develop by direct invasion of the valve rings of the heart near the vegetations. These are common with pyogenic cocci e. These vegetations are usually soft and friable and only loosely attached to the endocardium and they break off to form arterial emboli. These emboli can severely affect perfusion of the tissue down stream to the embolus causing infarcts in the tissues. Apart from the propensity to generate emboli, there is no correlation between size of vegetation and severity of endocarditis.
There are four consequences to the formation of the valvular vegetations. Diagnosis of subacute endocarditis can be very difficult and is oftentimes misdiagnosed. Acute endocarditis can rapidly cause irreversible damage to the heart valves and needs to be diagnosed and aggressively treated.
The following tests will help in confirming the diagnosis of endocarditis. Transesophageal echocardiography TEE is the most sensitive and can detect vegetations as small as 3 mm.
It readily detects extra-valvular extension of infection and can visualize valve perforations. Doppler color flow analysis allows for assessment of valve function, myocardial contractility and chamber volume.
This information is important in deciding if surgery is needed. Chest radiographs may demonstrate distinct round cannonball-like pulmonary emboli in right-sided endocarditis. Pulmonary edema may be present in those with acute mitral regurgitation or decompensated left-sided heart failure due to aortic valve regurgitation. Infective endocarditis is associated with a constant low-level bacteremia. Obtain 3 blood samples at least 10 ml of blood at least 15 minutes between each blood letting over a hour period.
The degree of late gadolinium enhancement of the pericardium, may be especially helpful in identifying patients in whom constriction will reverse or resolve. Low voltage and electrical alternans on the ECG suggest cardiac tamponade, but these findings lack sensitivity and specificity. When tamponade is suspected, echocardiography is done unless even a brief delay might be life threatening.
Then pericardiocentesis is done immediately for diagnosis and treatment. On an echocardiogram, respiratory variation of transvalvular and venous flows and compression or collapse of right cardiac chambers in the presence of a pericardial effusion support the diagnosis. Significant cardiac tamponade is a clinical diagnosis; echocardiographic findings alone are not an indication for pericardiocentesis.
If tamponade is suspected, right heart Swan-Ganz catheterization may be done. In cardiac tamponade:. Diastolic pressures are elevated about 10 to 30 mm Hg and equal in all cardiac chambers and in the pulmonary artery.
After pericarditis is diagnosed, tests to determine etiology and the effect on cardiac function are done. In a young, previously healthy adult who presents with a viral infection and acute pericarditis, an extensive evaluation is usually unnecessary. Differentiating viral from idiopathic pericarditis is difficult, expensive, and generally of little practical importance. In other cases, a biopsy of pericardial tissue or aspiration of pericardial fluid may be needed to establish a diagnosis.
Acid-fast stains and cultures of pericardial fluid are essential if tuberculosis TB is considered possible TB pericarditis can be aggressive and can worsen rapidly with corticosteroid therapy. Samples are examined for malignant cells. However, complete drainage of a newly identified pericardial effusion is usually unnecessary for diagnosis.
The choice between needle pericardiocentesis and surgical drainage depends on institutional resources and physician experience, the etiology of the effusion, the need for diagnostic tissue samples, and the prognosis of the patient. Needle pericardiocentesis is often best when the etiology is known or the presence of tamponade is in question. Surgical drainage is best when the presence of tamponade is certain but the etiology is unclear.
Laboratory tests of pericardial fluid other than culture and cytology are usually nonspecific. But specific diagnoses are sometimes possible using newer visual, cytologic, and immunologic analysis of fluid obtained via pericardioscopic-guided biopsy.
Cardiac catheterization may be useful for evaluating pericarditis and identifying the cause of reduced cardiac function. Other tests include complete blood count, acute-phase reactants, routine chemistry tests, cultures, autoimmune tests, and, when appropriate, tests for HIV, histoplasmosis complement fixation in endemic areas , and antibody tests for coxsackievirus, influenza virus, echovirus, and streptococcus. A purified protein derivative PPD skin test is done, but it can give false negative results; TB pericarditis can be ruled out only by culture of pericardial fluid for acid-fast bacilli.
Circ Cardiovasc Imaging , Nonsteroidal anti-inflammatory drugs NSAIDs , colchicine , and, infrequently, corticosteroids for pain and inflammation.
Hospitalization is warranted for some patients with an initial episode of acute pericarditis, particularly those with moderate or large effusions or with high-risk features, such as elevated temperature, subacute onset, immunosuppression, recent trauma, oral anticoagulant therapy, failure to respond to an initial course of aspirin or NSAIDs, and myopericarditis.
Hospitalization is needed to determine etiology and to observe for the development of cardiac tamponade. Close, early follow-up is important in patients who are not hospitalized.
Possible causative drugs eg, anticoagulants, procainamide , phenytoin are stopped. For cardiac tamponade, immediate pericardiocentesis see figure Pericardiocentesis Pericardiocentesis Pericarditis is inflammation of the pericardium, often with fluid accumulation. Except in emergencies eg, cardiac tamponade , pericardiocentesis, a potentially lethal procedure, should be done using echocardiographic guidance in a cardiac catheterization laboratory and should be supervised by a cardiologist or thoracic surgeon if possible.
Resuscitation equipment must be at hand. IV sedation eg, morphine 0. Under aseptic conditions, the skin and subcutaneous tissues are infiltrated with lidocaine.
A mm short-beveled, gauge needle is attached via a 3-way stopcock to a or mL syringe. The pericardium may be entered via the right or left xiphocostal angle or from the tip of the xiphoid process with the needle directed inward, upward, and close to the chest wall.
The needle is advanced with constant suction applied to the syringe. Echocardiography may be used to guide the needle as agitated saline is injected through it. Echocardiography is also increasingly used to identify the optimal puncture site and the needle trajectory. Once in place, the needle should be clamped next to the skin to prevent it from entering further than necessary and possibly puncturing the heart or injuring a coronary vessel.
ECG monitoring is essential for detecting arrhythmias produced when the myocardium is touched or punctured. As a rule, right atrial pressure and pulmonary artery occlusion pressure pulmonary capillary wedge pressure are monitored. Fluid is withdrawn until intrapericardial pressure falls below right atrial pressure, usually to subatmospheric levels.
If continued drainage is needed, a plastic catheter may be passed through the needle into the pericardium and the needle withdrawn. The catheter may be left in place for 2 to 4 days. Pain can usually be controlled with colchicine or aspirin to mg orally every 4 to 6 hours or other NSAIDs eg, ibuprofen to mg orally every 6 to 8 hours.
Severe pain may require opioids. Colchicine 0. Although most mild cases of idiopathic and viral pericarditis respond well within a week, the optimal duration of treatment is unclear. Typically, patients should be treated at least until any effusion and evidence of inflammation eg, erythrocyte sedimentation rate, C-reactive protein levels have resolved. An alternative approach is the use of prednisone at a lower dose 0. Tuberculous and pyogenic pericarditis should be excluded before corticosteroid therapy is initiated.
Anticoagulants are usually contraindicated in acute pericarditis because they may cause intrapericardial bleeding and even fatal tamponade; however, they can be given in early pericarditis complicating acute MI. Uncommonly, pericardial resection is required. If these drugs do not suffice, corticosteroids may be tried, presuming the cause is not infectious.
Refractory cases have been treated with interleukin-1 receptor antagonists eg, anakinra. In postpericardiotomy syndrome, post-MI syndrome, or idiopathic pericarditis, antibiotics are not indicated.
When required to control pain, fever, and effusion, prednisone 20 to 60 mg orally once a day may be given for 3 to 4 days. If the response is satisfactory, the dose is gradually reduced, and the drug may be stopped in 7 to 14 days. But sometimes many months of treatment are needed. Beginning on postoperative day 3, colchicine 1 mg orally once a day for 30 days, after a 2 mg load may reduce the incidence of postpericardiotomy syndrome after cardiac surgery. Aspirin should be used when pericarditis occurs in patients with an acute myocardial infarction.
For pericarditis due to rheumatic fever, another connective tissue disorder, or tumor, therapy is directed at the underlying process. For pericardial effusion due to trauma, surgery is sometimes required to repair the injury and remove blood from the pericardium. Pericarditis due to uremia may respond to increased frequency of hemodialysis, aspiration, or systemic or intrapericardial corticosteroids.
Intrapericardial triamcinolone may be useful. Chronic effusions are best treated by treating the cause, if known. Recurrent or persistent symptomatic effusions may be treated with balloon pericardiotomy or a surgical pericardial window. Asymptomatic effusions of unknown cause may require only observation. Congestion in chronic constrictive pericarditis may be alleviated with salt restriction and diuretics.
Digoxin is indicated only if atrial arrhythmias or ventricular systolic dysfunction is present. Patients with symptomatic constrictive pericarditis eg, with dyspnea, unexplained weight gain, a new or increased pleural effusion, or ascites and those with markers of chronic constriction eg, cachexia, atrial fibrillation, hepatic dysfunction, pericardial calcification usually require pericardial resection.
However, patients with mild symptoms, heavy calcification, or extensive myocardial damage may be poor surgical candidates. Left ventricular failure causes shortness of breath and fatigue, and right ventricular failure causes peripheral and abdominal fluid Patients who have constrictive pericarditis due to irradiation or a connective tissue disorder are especially likely to have severe myocardial damage and may not benefit from pericardial resection. Patients with newly diagnosed constrictive pericarditis who are hemodynamically stable and without evidence of chronic constriction may be given a 3-month trial of anti-inflammatory drugs, rather than pericardiectomy.
Patients with pericardial inflammation on MRI may also benefit from a trial of medical therapy first, rather than pericardiectomy.
Electrocardiography and echocardiography are usually adequate for diagnosis, but right and left heart catheterization, CT, or MRI may be needed to diagnose constrictive pericarditis. Effusions usually respond to treatment of the cause, but recurrent or persistently symptomatic effusions may require drainage percutaneous or surgical. Symptomatic chronic constrictive pericarditis usually requires pericardial resection, although patients with early stage constrictive pericarditis can be treated with a trial of medical therapy first.
From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Manual was first published in as a service to the community. Learn more about our commitment to Global Medical Knowledge. This site complies with the HONcode standard for trustworthy health information: verify here. Common Health Topics. Videos Figures Images Quizzes Symptoms. Symptoms and Signs. Acute pericarditis Pericardial effusion Cardiac tamponade Constrictive pericarditis.
Acute pericarditis Pericardial effusion Constrictive pericarditis Cardiac tamponade Diagnosis of cause Diagnosis reference.
Key Points. Myocarditis and Pericarditis. Test your knowledge. Aortic stenosis AS occurs when the aortic valve narrows, obstructing blood flow from the left ventricle to the ascending aorta during systole. There are several different causes of AS, and the causes differ among age groups.
However, in low and middle income countries, which of the following is the most common cause of AS in all age groups? More Content. Clinically, this presents predominantly as right-sided congestion jugular venous distention, edema, and ascites. Elevation in pulmonary capillary wedge pressure and a decreased cardiac output response to exercise given inadequate ventricular filling results in dyspnea and effort intolerance, although frank pulmonary edema is less common than typical systolic heart failure.
This in turn decreases the LV end diastolic volume LV preload and therefore left-sided stroke volume. Given a fixed pericardial volume in CP, pericardial coupling is greatly exaggerated, leading to dramatic ventricular interdependence. Abnormal ventricular septal motion results from enhanced respirophasic alterations in left- and right-sided stroke volume. In CP, due to the heart being encased by a noncompliant pericardium, the normal inspiratory decrease in intrathoracic pressure is not transmitted to intracardiac pressures.
This effect amplifies inspiratory decreases in pulmonary venous pressure since pulmonary veins are primarily extrapericardial , translating to a reduced left-sided inspiratory preload, further reducing left-sided inspiratory stroke volume. Multimodality diagnostic evaluation of CP highlights these findings, facilitating the diagnosis.
The low prevalence of CP makes identifying key physical examination and historical features an important initial step in the diagnostic process. A history of cardiac surgery, radiation or tuberculosis should heighten clinical suspicion in the presence of edema, abdominal distention and exertional dyspnea. Elevated jugular venous pressure JVP is present in virtually all patients that are not hypovolemic. Pericardial constraint results in the inability of the right heart to accommodate inspiratory abdominal venous return, translating to an inspiratory increase in the JVP Kussmaul's sign.
In contrast, restrictive cardiomyopathy demonstrates blunting of the x descent, due to impaired atrial relaxation and atrial myopathy. Auscultation may disclose a high pitched pericardial knock along the left sternal border.
Ascites and significant lower edema are common and often lead to the misdiagnosis of liver disease if the JVP findings are not recognized. Laboratory testing in CP is nonspecific. A high BNP can suggest a greater likelihood of restrictive cardiomyopathy, but studies have shown great overlap in diagnostic values in this population limiting clinical utility.
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