Pericardial disease is classified into three categories: pericarditis, pericardial effusion, and pericardial tamponade. The pathophysiologic importance of this constellation of disorders is related to the degree of compromise of cardiac ejection capabilities. Pericarditis is defined as inflammation of the pericardium; pericardial effusion is excess fluid in the pericardial sac, which reduces venous return and cardiac output; and pericardial tamponade is a condition in which pericardial fluid almost completely obstructs venous return and no blood is ejected (Tsolakis et al., 2004). Cardiac arrest, the consequence of pericardial tamponade, reflects the absence of blood in the heart that can be ejected with contraction.
The intrapericardial pressure normally is negative, and the elastic recoil of the pericardial sac permits the heart to fill with blood returning from the venous system. As fluid accumulates in the pericardial space, the pressure becomes more positive and venous return is impaired. As fluid accumulates in the pericardial sac, at a certain point the intrapericardial pressure matches the pressure of returning venous blood, and no blood is allowed to enter the heart. Without returning blood, cardiac output declines, leading to pump failure and cardiac arrest.
In a slowly developing effusion, cardiac ejection failure occurs later, allowing for a larger amount of effusion and a slow onset of what appears to be right heart failure. Most malignant effusions occur slowly and manifest in this manner, notoriously causing higher volume effusions. In the early phases of effusion, venous congestion can cause edema and hepatomegaly. As ventricular filling becomes more impaired, left ventricular output is reduced.
Several physiologic mechanisms can cause additional production of pericardial fluid, abnormal recirculation of fluid, or leakage of other fluids (e.g., blood) into the pericardial space. Pericardial fluid disorders may be infectious, transudative, and hemorrhagic. They may be related to medical disorders, surgery, trauma, or malignancy.
Pericardial effusions are further classified as transudative or exudative by the fluid characteristics (Maisch et al., 2004). Maisch and colleagues (2004) described transudative effusions caused by disorders of capillary permeability as having low LDH and protein levels, a low fluid to serum LDH ratio, and a low serum to fluid protein ratio. Transudative effusions are more commonly associated with nonmalignant effusions, although they may be present when large tumors obstruct recirculation of pericardial fluid.
Exudative effusions occur when an inflammatory stimulus is present. These effusions are characterized by an LDH level greater than 200 units/L, a protein level greater than 35 g/dL, a fluid to serum LDH ratio greater than 0.6, and a fluid to protein ratio greater than 0.3. They are more typical of malignant involvement of the pericardial fluid (Maisch et al., 2004).
EPIDEMIOLOGY AND ETIOLOGY
The incidence and severity of pericardial effusion and tamponade, as well as the prognosis, depend on the etiology and rapidity of onset. Many pericardial effusive disorders are multifactorial, involving both malignant processes and unstable medical conditions. The incidence has been reported as high as 10% to 30% in patients with pericardial involvement of malignancy and large malignant tumors that obstruct pericardial fluid drainage, such as lung cancer (Flounders, 2003). In one study of patients at the end of life, pericardial effusion was associated with an approximate life expectancy of 2 to 8 months (Cullinane et al., 2004). Despite the shortened life expectancy, as many as 95% of patients can expect symptomatic relief with aggressive intervention (Lindenberger et al., 2003). Hemorrhagic effusions are rare in patients with cancer, but they have the most severe prognosis (Flounders, 2003).
RISK PROFILE
Malignancy involving the chest causes pericardial inflammatory responses that may or may not involve the pericardial fluid (Quraishi et al., 2005; Kabukcu et al., 2004).
Malignant invasion or metastases (Suman et al., 2004)
• Breast cancer, especially invasive ductal cancer involving the inner aspects of the breast (Pokieser et al., 2004)
• Primary lymphomatous involvement of the pericardium (Chaves et al., 2004; Giunta et al., 2004; Nakakuki et al., 2004)
• Renal cell cancer
• Sarcoma—clear cell sarcoma, angiosarcoma (Frankel, 2004; Corso et al., 2003)
• Malignant melanoma
• Mesothelioma (Suman et al., 2004)
• Multiple myeloma (particularly related to amyloidosis) (Abelman et al., 2005; Zeiser et al., 2005; Arat et al., 2002)
• Gastric cancer
• Ovarian cancer
• Sarcoma—osteogenic sarcoma, angiosarcoma (Siddiqui & Al-Diab, 2003)
• Malignant thymoma (Gupta & Mathur, 2003)
Thoracic lymphatic obstruction
• Lymphoma (Giunta et al., 2004; Nakakuki et al., 2004)
• HIV disease (Barbaro, 2003; Gowda et al., 2003)
• Leukemia—especially acute lymphocytic leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia (Breccia et al., 2005; Chaves et al., 2004; Kadikoylu et al., 2003; Arya et al., 2002).
• Extramedullary multiple myeloma (Abelman et al., 2005; Zeiser et al., 2005).
Disorders of capillary permeability that occur with high-dose therapy.
• Radiation of at least 3000 cGy involving at least 33% of the heart, heart fractions exceeding 300 cGy per day (Shelton, 2006; Retter, 2002).
• Cyclophosphamide
• Cytosine arabinoside (Gahler et al., 2003)
• Gemcitabine (Vogl et al., 2005)
Disorders of capillary permeability that occur with immune activation therapies.
• Granulocyte-macrophage hematopoietic growth factor (GM-CSF)
• All-transretinoic acid (ATRA) (Datta & Gerardi, 2003; Larson & Tallman, 2003)
• Imatinib (Breccia et al., 2005)
Nonmalignant medical conditions (Kabukcu et al., 2004).
• Cardiac myxoma
• Autoimmune diseases—myxedema, systemic lupus erythematosus, scleroderma, rheumatoid arthritis (Lin et al., 2003).
• Uremia
• Displaced central venous catheter with fluid infusion (Shields et al., 2003)
• Complications of bone marrow aspiration (Marti et al., 2004)
Infections: Pericardial effusion is particularly common with infections that cause lymphadenopathy of mass effect (Kabukcu et al., 2004; Quraishi et al., 2005; Janoskuti et al., 2003; Levy et al., 2003).
• Bacteria: Actinomyces, Streptococcus pneumoniae, Citrobacter freundii, Coxiella burnetii, Nocardia spp., Serratia spp. (Janoskuti et al., 2004a; Levy et al., 2003)
• Fungi: Candida albicans (Rabinovici et al., 1997).
• Opportunistic organisms: Legionella pneumophila, Mycoplasma pneumoniae, Mycobacterium tuberculosis, toxoplasmosis
• Viruses
PROGNOSIS
Pericardial effusion and tamponade usually are indicative of severe, advanced chest malignancy and a poor prognosis. Most patients live less than 1 year after diagnosis of pericardial disease (Cullinane et al., 2004; Bastian et al., 2000), although the severity of the underlying malignancy has been reported to be one of the most important factors for predicting survival (Dosios et al., 2003). Additional predictive factors of a poor outcome are large amounts of pericardial fluid and a diagnosis of HIV infection (Foster, 2000). Patients with a capillary permeability–related disorder have a better prognosis, depending on the reversibility of the etiologic factor.
PROFESSIONAL ASSESSMENT CRITERIA (PAC)
Clinical signs and symptoms
1. The severity of symptoms may reflect the rapidity of onset. Slower developing effusions allow the body to adjust to progressive reductions in venous return, therefore these patients may not become severely symptomatic until several hundred milliliters have accumulated. Sudden pathologies may produce symptoms of tamponade with as little as 50 mL.
2. Dyspnea is the most common presenting symptom of malignancy-related pericardial disease (Chiu et al., 2004; Gibbs et al., 2000).
3. Symptoms of venous congestion from impeded venous return include edema, hepatomegaly, splenomegaly, positive hepatojugular reflex, bilateral jugular venous distention, and increased central venous pressure.
4. Signs and symptoms of increased pericardial pressure include bradycardia/heart block with inspiration, hypotension with narrow pulse pressure (closing the difference between the systolic and diastolic blood pressures), and pulsus paradox (Box 5-1).
BOX 5-1
MEASUREMENT OF PULSUS PARADOX
Clinical Pearls
1. Pulsus paradox is best assessed by the hemodynamic waveform of an arterial line. This allows the variation in blood pressure that occurs on inspiration and expiration to be measured on printed waveforms with graph grid lines.
2. Pulsus paradox is inaccurately assessed by automatic blood pressure devices.
3. The true paradox is determined during inspiration, when venous return is lowest.
Technique
1. Inflate the blood pressure cuff 15 to 20 mm Hg above the systolic pressure.
2. Slowly deflate the cuff until Korotkoff’s sounds are heard on expiration (higher systolic pressure) (e.g., 140 mm Hg).
3. Continue to deflate the cuff slowly until sounds are detected equally on inspiration and expiration. During the paradox, sounds may fade on inspiration and return on expiration. When the sounds are equal on inspiration and expiration, note this value (lower systolic pressure) (e.g., 120 mm Hg).
4. Subtract the lower pressure reading from the higher pressure reading to determine the degree of paradox (e.g., 140 − 120 = 20 mm Hg).
Determining the Significance of Findings
1. Paradox greater than 10 mm Hg indicates high thoracic pressure, although it is not specific for pericardial disease.
2. The paradox is more pronounced in patients who have lung masses or who are profoundly dehydrated.
5. Signs of decreased cardiac output include weak, thready distal pulses; cool, clammy extremities; cyanosis; oliguria; and diminished bowel sounds.
6. Pericardial rub is unusual with effusion and tamponade but may be present with pericarditis. It results from inflammation of the visceral and parietal pericardium with displacement of the fluid normally in that space. A rub present with pericardial effusion is related to high-volume effusions with uneven distribution of fluid and the presence of areas without fluid lubrication.
7. Because blood coming from the heart feeds the upper branches of the aortic arch first, patients have better upper extremity pulses than lower extremity pulses.
Radiologic tests
1. The chest x-ray film may show an enlarged cardiac silhouette, and the mediastinum may have a “water bottle” appearance (indicative of accumulation of more than 250 mL fluid). However, the x-ray findings may be inconclusive if the effusion is primarily anteroposteriorly displaced (Goyle & Walling, 2002).
2. A chest computed tomography (CT) scan may show an enlarged cardiac silhouette. It also may differentiate pericardial fluid from a hypertrophied myocardium. If CT scans are done, pericardial disease is more likely to be an incidental finding, because a definitive diagnosis can be made using bedside diagnostic tests.
Other diagnostic tests
1. The two-dimensional echocardiogram is the gold standard for diagnosis of pericardial effusion and tamponade (Spodick, 2003).
• Right ventricular collapse with impaired filling occurs with severe pericardial effusions.
• When the left ventricle fails to expand and fill with blood, cardiac arrest is imminent.
• The ejection fraction can be estimated and the urgency for treatment can be determined by the results of the echocardiogram.
2. A 12-lead electrocardiogram (ECG) may produce a number of nonspecific findings that, when they occur simultaneously, increase the likelihood that pericardial disease is present.
• Early changes in pericarditis or small pericardial effusions may include depressed P waves and nonspecific ST changes, although T-wave inversions are less common than with acute myocardial infarction (Kudo et al., 2003; Goyle & Walling, 2002).
• Early pericarditis is characterized by ST elevations in all the precordial ECG leads. Myocardial ischemia however, is an uncommon finding; in a study by Kudo and colleagues (2003), it was detected in fewer than 10% of patients with pericardial effusion.
• As pericardial effusion develops, the QRS voltage across all leads decreases and an axis deviation may occur. Low voltage is seen in approximately one fourth of patients with pericardial effusion, although its presence does not necessarily predict the volume or severity of the effusion (Kudo et al., 2003).
• The classic ECG finding associated with impending pericardial tamponade is electrical alternans, in which the R wave alternates between upward and downward deflection. This happens because the heart floats in a fluid casing, causing it to move in relation to the chest wall leads recording its activity (Billakanty & Bashir, 2006; Calkins & Amsterdam, 2004; Goyle & Walling, 2002; Lau et al., 2002).
3. Few laboratory abnormalities are indicative of pericardial disease. None are used to diagnose these disorders, but they may be used to monitor the response to treatment.
• Pericarditis may produce laboratory results that indicate an inflammatory process, such as elevation of the white blood cell count or the erythrocyte sedimentation rate.
• Pericarditis may cause an ischemic “troponin leak” that presents as increased serum troponins despite relatively normal CPK levels.
• Cytopathology of the pericardial fluid may detect malignant cells. This may assist treatment planning, although the yield is low. Combining cytopathology with fluorescence in situ hybridization (FISH) improves the clinical yield of positive pathologic markers (Gornik et al., 2005; Fiegl et al., 2004; Wang et al., 2000).
NURSING CARE AND TREATMENT
Emergency management of symptomatic pericardial effusion or impending pericardial tamponade
1. Administration of high-volume intravenous fluids (150 to 500 mL/hr) as centrally as possible can increase venous pressure above that of the pericardium. Increased venous pressure that exceeds pericardial pressures allows blood to flow into the heart, permitting blood ejection and improving cardiac output.
2. Oxygen therapy should be provided to maximize oxygen delivery to the tissues. The preferred administration is via mask. Assisted ventilation in any way (Ambu bag, endotracheal intubation with mechanical ventilation) changes to a positive pressure mode of ventilation, which will further reduce venous return in an already severely compromised patient (Faehnrich et al., 2003).
3. The patient should be positioned upright to ease dyspnea.
Definitive strategies to remove pericardial fluid
1. Emergency pericardiocentesis is reserved for unique circumstances in which the risk factors are not recognized until tamponade is present. Whenever possible, needle pericardiocentesis should be guided by fluoroscopy or echocardiogram. If rapid validation of the needle’s location is not possible, an alligator clamp can be used to link the ECG machine lead and the aspiration needle. If an acute, severe ST elevation occurs when the needle touches the myocardium, the operator can retract the needle fractionally before withdrawing fluid; this helps ensure that pericardial fluid is removed.
2. Pericardial catheter drainage allows for short-term, continuous drainage of the pericardium.
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• This technique allows immediate alleviation of symptoms, assessment of fluid characteristics, and a period of time to reverse the etiologic factors before the catheter is removed.
• Pericardial catheter drainage is indicated for hemodynamically unstable pericardial effusions. The complication rate is 4% to 17% (Allen et al., 1999).
• In nonmalignant conditions, the catheter is less likely to be left in the pericardial sac.
• The catheter may be a hard catheter, similar to a central line, or a soft, Silastic pigtail catheter, such as a long-term indwelling intravenous line.
• Care of the patient with a pericardial catheter is not well-documented. Impeccable infection precautions are necessary to ensure that catheter-related infection does not occur. A general review of patient care is included in Box 5-2.
BOX 5-2
NURSING MANAGEMENT OF A PERICARDIAL CATHETER
Assessment
1. Catheter patency and drainage: Production of continuous small amounts of serous drainage is normal. If the drainage suddenly stops, the patient should be assessed for signs and symptoms of recurrent pericardial effusion. Increased drainage after catheter insertion and initial drainage is rare.
2. Drainage characteristics: Drainage usually is serous or serosanguineous, but it does not usually clot. Amounts normally are less than 100 to 200 mL/day.
3. Exit site: The catheter exit site is assessed for irritation or for drainage that is evidence of infection.
4. Catheter placement: The catheter often is sutured in place, but it can be displaced by sliding out. The length of catheter outside is measured and compared to the baseline every shift. Migration of the catheter outward helps document displacement. Catheter migration into the body occurs less often; it may be indicated by changes in the catheter measurement or by a new onset of dysrhythmias.
5. Evidence of recurrent pericardial effusion/tamponade: If excess pericardial fluid is produced or drainage is blocked, the trapped fluid in the pericardial sac causes recurrent symptoms of effusion and impending tamponade (i.e., bilateral jugular venous distention, pulsus paradox, muffled heart sounds, diminished point of maximal impulse, and reduced extremity pulses). Assessment for the presence or absence of these symptoms may be done every shift; however, this assessment is most important if the drainage is diminished.
