Notas finales sobre la evaluación de un sistema de PR basado en la equivalencia química

examination, and electrocardiography.

▪ Pericardial disease can compromise cardiac output through either cardiac tamponade or constrictive pericarditis.

▪ Cardiac tamponade should be suspected when hypotension, elevated jugular venous pressure, and muffled heart sounds develop in a patient with recent cardiac surgery, aortic dissection, myocardial infarction, or acute pericarditis. The diagnosis is supported by echocardiographic evidence of effusion, right ventricular diastolic collapse, and variation in transmitral and transtricuspid Doppler flow velocities.

The pericardium can be affected in a vast array of diseases, both primarily and secondarily. The most common clinical manifestation of pericardial involvement is inflammation, causing acute pericarditis. The other clinical manifestation of pericardial disease is hemodynamic compromise, resulting from either cardiac tamponade or constrictive pericarditis. This chapter reviews the diagnosis, evaluation, and treatment of these disorders.

Acute Pericarditis

I. EPIDEMIOLOGY

1. Accurate estimation of the incidence and prevalence of acute pericarditis is limited by underdiagnosis but may account for up to 5% of presentations for nonischemic chest pain.

2. Acute inflammation of the pericardium can be an isolated process but more commonly is the result of another systemic condition ( Box 13-1 ).

3. Therapeutic radiation, percutaneous interventions, cardiothoracic instrumentation, and human

immunodeficiency virus infection are becoming more prevalent causes of pericarditis in Western populations. Worldwide, however, mycobacterial disease remains the most common cause of pericarditis.[1]

BOX 13-1

COMMON CAUSES OF ACUTE PERICARDITIS Idiopathic (often thought to be viral)

Infection

Common: cardiotropic viruses, gram-positive bacteria, Mycobacterium tuberculosis Less common: fungi, parasites, spirochetes, rickettsiae

Metabolic

Renal failure Hypothyroidism Neoplastic

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II. CLINICAL PRESENTATION

Acute pericarditis classically presents with sharp pleuritic chest pain that is progressive. Often the pain is relieved by sitting up or leaning forward and exacerbated when lying supine. The chest discomfort may radiate to the neck, arms, shoulder, and trapezius muscle ridge. The physician must hunt diligently for associated symptoms, which may be nonspecific signs of viral infection or systemic inflammation (including nonproductive cough, fever, and myalgias). III. DIAGNOSIS

A. PHYSICAL EXAMINATION

1. The hallmark physical examination finding is a pericardial friction rub, heard in approximately 85% of patients with acute pericarditis.[2] The friction rub is “scratchy,” superficial, and heard loudest in end-expiration with

the patient leaning forward. The sound can be easier to detect and differentiated from pleural sounds if the patient suspends respirations. Classically, the rub has a triple cadence with atrial systolic, ventricular systolic, and early diastolic components. Often it is biphasic or monophasic, especially in patients with atrial or

ventricular tachycardia, because of fusion of approximate sounds.

2. Electrocardiography. Although the pericardium itself has no detectable electrical activity, pericardial inflammation can lead to electrical changes in the epicardial tissue, which are detected by the surface electrocardiogram.

a. The electrocardiographic changes associated with this epicardial inflammation typically evolve through four stages, which, when collectively present, are typical of pericarditis ( Fig. 13-1 ).

(1) Phase I.

(a) Diffuse ST elevation (except for aVR).

(b) PR depression in the inferolateral leads (II, III, aVF, V5, V6). (2) Phase II. ST and PR segment normalization.

(3) Phase III. Diffuse T wave inversions (occasionally not present).

(4) Phase IV. Resolution of electrocardiographic changes or persistence of T wave inversions, indicating “chronic” inflammation.

b. The electrocardiographic changes must be differentiated from acute myocardial infarction and other causes of ST elevation (see Chapter 6 ).[3] Pericarditis typically does not involve Q waves, hyperacute T waves, and QT prolongation.

c. Low electrocardiographic voltage and electrical alternans are insensitive indicators of small to moderate pericardial effusion, and when present they indicate a large effusion. When they are coupled with sinus tachycardia, pericardial tamponade should be suspected.

3. Echocardiography may be unremarkable (dry pericarditis) or show pericardial effusion.

4. The chest radiograph may show a newly enlarged cardiac silhouette and an associated pleural effusion, usually left sided.

5. Laboratory evaluation should include evaluation of renal function, erythrocyte sedimentation rate, C-reactive protein (CRP), antinuclear antibodies, lactate dehydrogenase, and complete blood cell count. Blood cultures should be drawn in febrile patients. Tuberculin skin test and evaluation of human

immunodeficiency virus status are warranted. Routine viral studies are not indicated because they do not change management. Creatine kinase, creatine kinase myocardial band, and troponin should always be followed to rule out ischemia. In viral or idiopathic pericarditis, troponin elevation is common, but unlike acute coronary syndromes it is not a negative prognostic marker.[4]

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FIG. 13-1 Electrocardiographic changes with acute pericarditis.

IV. ETIOLOGY AND MANAGEMENT

The differential diagnosis of acute pericarditis is broad and diverse. The most common etiological categories are infectious, metabolic, rheumatic, neoplastic, and diseases of contiguous organs, most commonly myocardial infarction. Management is dictated by the cause of the effusion and the presence and extent of hemodynamic compromise.

A. INFECTIOUS PERICARDITIS

1. Viral infections are the most common cause of infectious pericarditis, including coxsackie virus, influenza virus, human immunodeficiency virus, and the hepatitis A and B viruses. Clinical presentation is that of a viral syndrome with fever and leukocytosis. Nonsteroidal antiinflammatory drugs (NSAIDs) are the mainstay of therapy. Approximately 50% of patients have recurrence within 8 months, and, uncommonly, chronic inflammation develops.

2. In recurrent idiopathic pericarditis, treatment is largely supportive. NSAIDs are occasionally helpful; however, colchicine offers the best prophylaxis against recurrence.

3. Bacterial infection of the pericardium is a more serious condition with significant morbidity and mortality.

a. The offending organisms usually are gram-positive pathogens, including staphylococci, streptococci, and pneumococci. Less commonly, and usually in the setting of an

immunocompromised state, other organisms such as Escherichia coli, Salmonella, Clostridium, and Neisseria have been implicated. Pericardial effusions make the pericardium particularly vulnerable to bacterial infection via hematogenous spread.[5] Similarly, surrounding bacterial infections, such as lobar pneumonia, mediastinitis, and bacterial endocarditis, predispose the pericardium to bacterial invasion.

b. Bacterial pericarditis has an acute presentation, usually with significant fever and pain. An inflammatory, exudative effusion almost always accompanies it.

c. Management involves intravenous antibiotics and drainage.[5] A combination of an

antistaphylococcal antibiotic and an aminoglycoside should be initiated. Subxiphoid surgical pericardiotomy is preferred over percutaneous procedures. Pericardiectomy is necessary in

patients with dense adhesions, loculated or thick effusion, recurrence of tamponade, or progression to constriction. [6] [7]

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4. Mycobacterium tuberculosis is particularly notable for its predilection for the pericardium. The illness usually arises in an indolent fashion, without evidence of extrapericardial tuberculous infection.

a. Diagnosis of tuberculous pericarditis can be difficult. Although identification of M. tuberculosis in pericardial fluid or tissue biopsy is specific, it is not sensitive. Extrapericardial tuberculosis and positive tuberculin skin tests can help support the diagnosis but are not confirmatory. The optimal test is M. tuberculosis DNA identification by polymerase chain reaction amplification in the pericardial fluid, which is 100% sensitive and more than 70% specific for tuberculous infection. [8] [9]

b. Management involves prompt therapy with combination of three to four tuberculostatic drugs for 9 to 12 months and a prednisone taper starting at 1 mg/kg for the first week and tapered over 8 weeks.[10]

B. METABOLIC DERANGEMENTS

1. Uremia can cause pericarditis in patients with chronic renal failure, on hemodialysis with inadequate

treatment, or less commonly with acute renal failure. No direct correlation exists between the level of uremia and clinical manifestations. Treatment focuses on hemodialysis to correct the uremia. Pericardiocentesis should be performed early in patients with pretamponade physiology given increased risk of vascular collapse with acute fluid removal during dialysis.

2. Pericarditis has been observed in other metabolic derangements, notably diabetic ketoacidosis,

hypothyroid myxedema, adrenal failure, gout, and hypercholesterolemia. [11] [12] A clear pathogenesis, other than systemic inflammation, has yet to be described in these conditions.[5]

C. RHEUMATIC DISEASES

1. The majority of vasculitides and connective tissue disorders can have associated pericarditis. The same pathologic process that leads to blood vessel and tissue inflammation also leads to pericardial inflammation.

2. Rheumatoid arthritis is the most common rheumatologic disease associated with pericarditis, usually with fibrinous exudates. Systemic lupus erythematosus is also commonly associated with pericarditis as well. The pericardial inflammation tends to parallel systemic flares.

D. NEOPLASTIC DISEASE

1. Pericardial disease caused by primary pericardial neoplasms, mesotheliomas, and sarcomas is rare and typically develops in the third and fourth decades of life.[5]

2. Neoplastic involvement of the pericardium can occur through metastatic disease, usually via pericardial lymphatics, or from direct extension of malignant tissue from breast, lung, or chest wall. Because

malignancies may initially manifest themselves as “idiopathic” pericarditis, a search for systemic neoplasms is warranted in certain situations. [13] [14]

3. Management of neoplastic pericardial disease includes pericardial drainage, typically with pericardial windows or shunts. Surgical resection is necessary for recurrent pericardial constriction from malignancy. Conservative therapy with pericardial sclerosis may be appropriate as palliative treatment in poor surgical candidates.[5]

E. MYOCARDIAL INFARCTION

1. Myocardial infarction can be associated with pericarditis, either early (< 7 days) or late (weeks to months) after infarction. Almost half of transmural infarctions are associated with early pericarditis.

2. Early postinfarction pericarditis increases in incidence with infarct size and is a common cause of new chest pain during the first few days after infarction. [5] [15] [16] In-hospital outcomes do not seem to be affected by early postinfarction pericarditis.

a. Use of NSAIDs should be avoided in the first 7 to 10 days after infarction because, like

corticosteroids, they have been linked to scar thinning, ventricular aneurysm, and free wall rupture, and they also increase aspirin resistance.

b. Early infarction pericarditis is not an absolute contraindication to anticoagulation, although caution should be used.

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3. Late postinfarction pericarditis, also known as Dressler syndrome, is more common with larger infarcts but can also be associated with nontransmural infarction. [5] [17] The syndrome arises between 1 week and several months after infarction and is thought to be immune mediated. Presentation tends to be

characteristic for acute pericarditis, and management is focused on antiinflammatory treatment with NSAIDs or corticosteroids, if necessary.