Pericardial, Myocardial, and Endocardial Disease

Pericardial, Myocardial, and Endocardial Disease

Margaret M. McNeill

Pericardial, myocardial, and endocardial diseases impact the health of populations across the globe, and can have a significant impact on cardiac function and therefore quality of life. These diseases translate into a tremendous economic burden; thus, it is therefore imperative for nurses to know the best practices for management of patients with pericardial, myocardial, and endocardial disorders in order to optimize patient outcomes.


The pericardium is a double-layered fibroserous sac that envelops the heart, covering almost the entire surface and part of the great vessels.1 The pericardium is composed of two layers, the serosa and the fibrosa, which contain nerves, blood vessels, and lymphatics. The fibrous outer layer, also called the parietal pericardium, is attached to the sternum, great vessels, and diaphragm. The phrenic nerves innervate most of the parietal pericardium. A serosal layer of cuboidal cells one-cell-layer thick lines the pericardium. The monocellular serosa directly covers the heart surfaces and is also known as the visceral pericardium or the epicardium. The pericardial space between the layers normally contains 15 to 35 mL of serous pericardial fluid produced by the visceral pericardial cells.2,3

The pericardium is a relatively inelastic covering and it exerts a powerful restraining effect on the size of the heart in situations of acute volume overload.2,4 The pericardium also exerts a mechanical effect that enhances normal ventricular interactions that contribute to the balance of right and left cardiac outputs.5 The pericardium maintains the heart in a stable position and functionally optimum shape within the mediastinum. It acts as a barrier to inflammation from contiguous structures and contains defensive immunologic components.5 The layer of pericardial fluid reduces friction on the epicardium and equalizes gravitational, hydrostatic, and inertial forces over the surface of the heart.6 While the pericardium serves several functions, cardiac activity is normal if the pericardium is missing due to congenital absence or surgical removal.

Almost every known medical and surgical pathologic process can contribute to pericardial disease, either primarily involving the pericardium or with an indirect impact.2 For unknown reasons, there is a predominance of men with pericardial disease.7 The spectrum of pericardial diseases ranges from congenital defects, pericarditis, neoplasms, and cysts.8 Pericarditis, pericardial effusion, and cardiac tamponade are the most important pericardial conditions to understand.


Pericarditis is the inflammation of the pericardium surrounding the heart. The acute inflammatory process can produce either serous or purulent fluid, or a dense fibrinous material.9 The possible sequelae of pericarditis include cardiac tamponade, recurrent pericarditis, and pericardial constriction.10

Acute clinically noneffusive or “drypericarditis refers to pericardial inflammation without a significant symptom-causing effusion, and is the most commonly recognized pericarditis. Acute inflammatory pericarditis usually lasts 1 to 3 weeks and does not lead to further problems. Acute effusive pericarditis is pericarditis in which an effusion is present in the pericardium.


Pericarditis is caused by many different conditions. The etiological classification of pericardial diseases comprises infectious pericarditis, pericarditis in autoimmune diseases, postmyocardial infarction syndrome, and auto-reactive (chronic) pericarditis.11 There has been a sharp decline in infectious pericarditis in the last few years, except in immunocompromised individuals, such as those with acquired immunodeficiency syndrome (AIDS).12

Viruses associated with pericarditis include influenza, coxsackie A or B, varicella, mumps, hepatitis B, mononucleosis, and human immunodeficiency virus (HIV).7 Idiopathic pericarditis is thought often to be the result of viral pericarditis where the virus is never identified. Bacterial infections, such as tuberculosis, are rare in the United States, but have surged in incidence in regions of the world where HIV and AIDS are epidemic. Other bacteria that cause pericarditis include Staphylococcus, Pneumococcus, and Streptococcus species. Aspergillosis and histoplasmosis are among the fungal infections that can cause pericarditis.

Frequently, the patient’s history indicates that a viral infection preceded the pericarditis. Sometimes the pericarditis itself is the first presenting symptom of a systemic disease, such as systemic lupus erythematosus or malignancy. In viral pericarditis, the pericardial fluid is most commonly serous, of low volume, and resolves spontaneously.9 Exudative, hemorrhagic, and leukocyte-filled large effusions may be associated with neoplastic, tuberculous, and purulent pericarditis.6

Assessment Findings

The onset of symptoms can be acute, as is commonly seen in viral pericarditis, or insidious, as seen in uremic pericarditis. Acute
viral pericarditis is nearly always preceded by a recent respiratory, gastrointestinal, or “flu-like” illness. A prodrome of fever, malaise, and myalgia is common in acute pericarditis, although older patients may not exhibit fever.1

A major symptom of pericarditis is chest pain that is retrosternal or left precordial, radiating to the trapezius ridge and varying with posture. The pain is transmitted through the phrenic nerves, and usually occurs on the left side. Shoulder pain should be distinguished from trapezius ridge pain by having the patient physically point to the specific site of pain. Frequently the chest pain caused by pericarditis induces shallow tachypnea as patients attempt to splint their chest movement.2 The pain is generally worse when lying supine and is relieved by sitting.

A pericardial friction rub is pathognomonic for pericarditis, but is frequently not present, may come and go, and can vary in quality and intensity. Auscultation for a pericardial friction rub is accomplished with the diaphragm of the stethoscope at the left middle to lower sternal border during both inspiration and expiration, while the patient changes positions.2 Often best heard at end expiration while the patient is leaning forward, the sound is classically a rasping or creaking with a triple cadence, but can also be bi- or monophasic.1

A diagnosis of acute pericarditis is made if the patient has a pericardial friction rub or chest pain, and widespread ST segment elevation on electrocardiography.10 It is important to differentiate pericarditis from myocardial infarction (MI) and pulmonary embolism. Table 30-1 describes the different features from these three conditions.10


Symptom and Clinical Finding

Myocardial Ischemia or Infarction


Pulmonary Embolism

Chest pain




Anterior, posterior, or lateral


Sudden, often waxing and waning




Pressure-like, heavy, squeezing

Sharp, stabbing, occasionally dull

Sharp, stabbing

Change with respiration


Worsened with inspiration

In phase with respiration (absent when the patient is apneic)

Change with position


Worse when patient is supine; improved when sitting up or leaning forward



Jaw, neck, shoulder, one or both arms

Jaw, neck, shoulder, one or both arms, trapezius ridge



Minutes (ischemia); hours (infarction)

Hours to day

Hours to day

Response to nitroglycerin


No change

No change

Physical examination

Friction rub

Absent (unless pericarditis is present)

Present (in 85% of patients)

Rare; a pleural friction rub is present in 3% of patients

S3 sound, pulmonary congestion

May be present




ST segment elevation

Convex and localized

Concave and widespread

Limited to lead III, aVF, and V1

PR segment depression




Q waves

May be present


May be present in lead III or aVF or both

T waves

Inverted when ST segments are still elevated

Inverted after ST segments have normalized

Inverted in lead II, aVF, or V1 to V4 while ST segments are elevated

Atrioventricular block, ventricular arrhythmias




Atrial fibrillation

May be present

May be present

May be present

The pericardium itself does not produce electrical activity. The electrocardiogram (ECG) changes seen in pericarditis are a result of superficial inflammation of the myocardium underneath the pericardium. The ECG of a patient with pericarditis may be normal, atypically abnormal with nonspecific changes, or have a fourstage sequence that is diagnostic. Figure 30-1 shows the electrocardiographic manifestations of pericarditis.

In stage I, there are ST segment deviations, primarily due to inflammation on the ventricular surfaces. PR segment deviations are also usually present. Stage I is virtually pathognomonic of acute pericarditis when it involves all or almost all leads with early ST junction elevations that produce an appearance of T waves “jacked-up” on the QRS interval, but that is otherwise normal.2 The ST segment is always depressed in aVR.4

In early stage II, the ST segments return to baseline, and PR segments may now be depressed. In late stage II, the T waves flatten and then invert. In stage III, the ECG is characteristic of diffuse myocardial injury. In stage IV, the ECG evolves back to the prepericarditis state.2 Stage IV may last days or months.4

The changes seen in the ECG of a patient with pericarditis can occur over hours, particularly from stages I to II, or can take place over days or weeks, most often as stage III evolves to stage IV. Because of more prompt recognition and treatment of pericarditis, not all stages may be exhibited.4 The ST elevation seen in pericarditis is usually distinguished from that of acute MI by the absence of Q waves, upward ST segments, and the absence of associated T wave inversion.13 In research examining the cause of ST segment abnormalities in emergency department
chest pain patients, pericarditis was found in 1% of the study population.14

Figure 30-1 ECG manifestations of pericarditis. (A) Typical, quasi-diagnostic stage I ECG: J (ST) elevated in all leads except AVL, depressed AVR and V1. PR segment deviated except in aVL where P is small. (B) Early stage II. J (ST) returning to baseline. (C) Stage III. T waves inverted in most leads and typically upright in aVRAVR and V1. (From Spodick, D. H. [1997g]. Electrocardiographic abnormalities in pericardial disease. In D. H. Spodick [Ed.], The pericardium: A comprehensive textbook [pp. 40-64]. New York: Marcel Dekker.)

Evaluation of laboratory results almost always reveals an elevated erythrocyte sedimentation rate. Leukocytosis is present early but, depending on etiology, may give way to lymphocytosis. Serum cardiac enzymes are frequently normal unless the myocardium is involved, and then they give some indication as to the degree of involvement. In a study on viral or idiopathic pericarditis, troponin I elevation was frequently observed (32% of cases) and associated with young age, male gender, ST segment elevation, and pericardial effusion at presentation.15 It is uncertain if elevated troponin I levels have any prognostic value.15

In some parts of the world, such as South Africa, tuberculosis is a major health problem, and can be complicated by tuberculosis
pericarditis. The need for early diagnosis has led to emphasis on biochemical tests such as the pericardial adenosine deaminase test, and the use of interferon as an indicator of pericardial disease due to tuberculosis.16

Echocardiography is critical to assess the pericardium in pericardial disease. Computed tomography (CT) and magnetic resonance imaging (MRI) allow examination of the entire chest, so abnormalities that might be related to the pericardial findings can be assessed.

Medical Management

The goal of treatment in acute pericarditis is to relieve pain and prevent complications.9 Treatment of the underlying cause is also a priority. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment. Ibuprofen is preferred by many clinicians due to its rare side effects, favorable impact on coronary flow, and large dose range.2 Depending on the severity and response, 300 to 800 mg every 6 to 8 hours may be initially required, and is best continued until the effusion is resolved, which may be days or weeks.11 Aspirin (325 to 650 mg four times a day) is also commonly used to treat pericarditis.3 Gastrointestinal protection during NSAID therapy is important.3,11,17 Colchicine (0.5 or 6 mg b.i.d.) added to an NSAID or as monotherapy also appears to be effective in initial episodes, and to prevent recurrences.11,12 Systemic corticosteroid therapy is recommended only in connective tissue diseases, autoreactive or uremic pericarditis.3,11 Intrapericardial corticosteroids have been effective and do not cause systemic side effects.11

Pericarditis due to bacterial infections such as tuberculosis is treated by directing treatment to the cause. The mainstay of treatment of tuberculosis pericarditis in Africa is the 6-month course of antituberculosis drugs recommended by the World Health Organization.18 Pericardiocentesis is recommended in all patients suspected of tuberculosis to facilitate diagnosis.19

Constrictive Pericarditis.

Constrictive pericarditis results from a scarred, and often thickened and calcified pericardium that limits diastolic ventricular filling.20 Tuberculosis is responsible for most cases of constrictive pericarditis in Africa and Asia.21 Other causes of constrictive pericarditis are idiopathic, postradiation, and postsurgical.22,23

The often thickened, adherent pericardium restricts ventricular filling and limits chamber expansion and maximal diastolic volumes. End-diastolic pressures in all heart chambers are typically elevated and equalized. During classic constriction, Kussmaul’s sign, inspiratory jugular venous distention, replaces the normal inspiratory venous “collapse” that reflects a normal inspiratory decrease of 3 to 7 mm Hg in right atrial pressure. This sign is a hallmark of constrictive pericarditis.2 Patients present with signs of heart failure, although pulmonary edema is usually not a feature.3,24

A calcified pericardium is often visible on chest x-ray film.25,26 CT, MRI, and echocardiography are tools also used to diagnose constrictive pericarditis.3 CT allows detection of calcification that occurs in restrictive pericarditis.5 Many abnormal findings can be seen on the echocardiogram that indicate constrictive pericarditis, such as premature opening of the pulmonic valve and rapid posterior motion of the left ventricular posterior wall in early diastole, with little or no posterior motion during the rest of diastole. However, these findings are not specific for constrictive pericarditis and can be caused by other conditions, such as restrictive cardiomyopathy (RCM).27,28

Pericardiectomy, surgical removal of the pericardium, is the treatment for symptomatic constrictive pericarditis.24 The procedure may be either a total or a partial pericardiectomy. In a recent study, total pericardiectomy was associated with lower perioperative and late mortality, as well as a better hemodynamic condition for the patient.22 Idiopathic etiology was associated with better outcomes in two studies.22,24

Recurrent Pericarditis.

Recurrent pericarditis is a complication of acute pericarditis. Recurrence is diagnosed by recurrent pain and one or more of the following signs: fever, pericardial friction rub, ECG changes, effusion on echocardiography, and elevation of white blood count, C-reactive protein level, or the erythrocyte sedimentation rate.17 The rate of recurrence is reported to vary from 15% to 50%. It is considered an autoimmune phenomenon.17 Imazio et al.17,29 found an increased risk of recurrence if corticosteroids were used during treatment of the first episode of pericarditis. Risk factors for recurrence in another study were identified as female gender, previous use of corticosteroids, and previous recurrent pericarditis.30 Use of colchicine along with NSAIDs during a first episode of pericarditis has been found to decrease recurrence.29

Approximately 20% of pericarditis patients have a recurrence within months, or rarely, within years.31 In a systematic review spanning 40 years of literature on patients with idiopathic recurrent pericarditis, the complication rate of pericardial tamponade was 3.5%, and no patients developed constrictive pericarditis.32

Pericarditis Associated With MI

Early Acute Post-MI Pericarditis.

In the immediate period after MI, an early pericardial syndrome may develop and then resolve over a period of approximately 1 week. Pericardial involvement is correlated to infarct size.33 The ECG shows a typical pattern of pericarditis and is helpful in differentiating between pericardial and ischemic pain. Pericardial friction rubs may be heard. As in all pericarditis, rubs are virtually 100% specific, but sensitivity depends on frequency of auscultation, because they tend to come and go over hours.12 The course is usually benign, and treatment consists of aspirin or other NSAIDs. Treatment of MI with thrombolysis and mechanical revascularization appear to have reduced the incidence of this form of pericarditis by at least 50%.33

Dressler’s Syndrome.

Dressler’s syndrome of chest pain, pleurisy, pericarditis with friction rub, severe malaise, moderate fever, and leukocytosis occurs 3 weeks to several months post-MI. The underlying pathologic process is unknown, but it is thought to reflect a late autoimmune reaction mediated by antibodies to circulating antigens.34 In contrast to early post-MI pericarditis, inflammation is diffuse and not localized to the myocardial injury site.33

Pericardial Effusion

Pericardial effusion is an increased amount of fluid within the pericardial space. This fluid can be serous, serosanguineous, pus, lymph, or blood.3


Many conditions cause acute pericarditis and pericardial effusions, including uremia, tuberculosis, neoplasms, and connective tissue diseases. The effusion may also be associated with
acute idiopathic pericarditis. Pericardial effusions occur with heart failure and LVH, and are also common after cardiac surgery. Effusions associated with cardiac surgery usually resolve after a month.6 In a population of patients in Italy, neoplastic etiology was found in 33 of 450 patients with acute pericardial disease (7.3%). Four percent of these patients presented with acute pericardial disease as the first manifestation of their malignancy.35 Pericardial effusions are also seen secondary to uremia of renal failure and hypothyroidism. In a population of patients in Turkey, uremic pericarditis resulting from poorly controlled renal failure due to economic considerations was the most common cause of pericardial effusion.20 Tuberculosis is responsible for approximately 70% of cases of large pericardial effusions in developing countries.21


The normal pericardium has a reserve capacity of 150 to 250 mL. An increase of volume of this amount in the pericardial space will not result in a major increase in intrapericardial pressure. Intrapericardial pressure will increase once this reserve volume is exceeded, and is also a function of how quickly the volume in the pericardial space accumulates. If fluid accumulates slowly, the normally stiff pericardium will stretch. However, if there is increased stiffness of the pericardium, as seen in constrictive pericarditis, small amounts of fluid will result in increased pericardial pressure. Once the intrapericardial pressure is elevated, the filling of the cardiac chambers becomes limited due to compression, resulting in hemodynamic effects.5 Figure 30-2 shows the difference in effects of rapid versus slow effusion accumulation.36

Figure 30-2 Cardiac tamponade. Pericardial pressure-volume (or strain-stress) curves are shown in which the volume increases slowly or rapidly over time. In the left-hand panel, rapidly increasing pericardial fluid first reaches the limit of the pericardial reserve volume (the initial flat segment) and then quickly exceeds the limit of parietal pericardial stretch, causing a steep rise in pressure, which becomes even steeper as smaller increments in fluid cause a disproportionate increase in the pericardial pressure. In the right-hand panel, a slower rate of pericardial filling takes longer to exceed the limit of pericardial stretch, because there is more time for the pericardium to stretch and for compensatory mechanisms to become activated.

Assessment Findings

A 2003 task force of the American College of Cardiology, the American Heart Association, and the American Society of Echocardiography gave the use of echocardiography for evaluation of all patients with suspected pericardial disease an evidence class I recommendation.37 Pericardial effusions are classified according to the distance between the left ventricular posterior wall and pericardium. Echocardiography can classify mild (<10 mm), moderate (10 to 20 mm), and severe (>20 mm) effusions.3,20 “Noncompressing” effusions do not produce changes in CO or pulsus paradoxus. If the effusions are caused by a systemic disease, then the symptoms are related to that disease. A pericardial rub may or may not be appreciated. The ECG shows reduced voltage, and these changes are nonspecific and unreliable for diagnosis. Cardiomegaly on chest x-ray film may be observed if effusion is present. If the effusion is visible on radiography, then there is at least 250 mL of fluid accumulated.2

Medical Management

Pericardial effusion can be treated medically, with pericardiocentesis or with surgery.20 Patients presenting for the first time with pericardial effusion are usually hospitalized to determine the cause of the effusion and to observe for the development of cardiac tamponade.34 Medical management involves treatment of the pericarditis as discussed above with NSAIDs. Conservative treatment with clinical and echocardiographic monitoring is usually the approach for small or moderate effusions.3 Uremic pericardial effusions are often treated with aggressive hemodialysis.20

Pericardiocentesis can be guided by fluoroscopy in the cardiac catheterization laboratory with ECG monitoring, or it can be conducted with echocardiography guidance.20 This procedure is generally reserved for emergency situations where the patient is exhibiting symptoms of hemodynamic compromise as in cardiac tamponade, or for diagnostic purposes when tuberculosis is suspected.

Subxiphoid pericardiostomy and tube drainage can be performed under general or local anesthesia with sedation. During this procedure a small 2- to 4-cm piece of the pericardium is excised under direct vision. This sample can be analyzed. This subxiphoid incision is closed, and through a separate incision, a soft chest tube is placed in the pericardial cavity lateral to the right ventricle from the pericardiotomy, for postoperative drainage.20

Transcutaneous pericardioscopy and catheter drainage is another procedure to treat pericardial effusions. In this procedure general anesthesia is not needed. There is no need for an incision and therefore there is less pain, and several samples of the pericardium can be taken. However, small or posterior effusions are difficult to manage with this procedure, and it requires a clinician with a great deal of experience with the procedure.20 Video-assisted transthoracic pericardial drainage, where a pericardial window is created, requires general anesthesia and single-lung ventilation. The window is not effective for longer-term drainage.20

Cardiac Tamponade

Cardiac tamponade is a life-threatening hemodynamic condition resulting from a pericardial effusion that has compressed the heart to restrict cardiac chamber filling. This restriction decreases cardiac output and causes heart failure. Cardiac tamponade can be caused by varying amounts of fluid. The speed of accumulation typically affects the severity of symptoms. Any scarring or thickening of the pericardium serves to amplify the effects of excess pericardial fluid on the heart.


The most common causes of cardiac tamponade include effusions secondary to neoplasm, idiopathic pericarditis, acute MI resulting in pericarditis and/or cardiac rupture, catheter- or pacemaker-induced perforation of the right heart, coronary vessel perforation during percutaneous interventions, and cardiac surgery.5 Trauma can also cause pericardial tamponade. Tamponade is reported in 15% of patients with idiopathic pericarditis but in as many as 60% of those with neoplastic, tuberculosis, or purulent pericarditis.38


Cardiac tamponade results from a pericardial effusion that increases intrapericardial pressure, compresses the heart, leading to diminished filling volumes and heart failure. If the effusion accumulates rapidly, as seen in trauma, then tamponade can occur with smaller volumes of 300 mL. Rapid accumulation does not allow time for the stiff pericardium to stretch. But an effusion that accumulates slowly, as seen in neoplasm, can be of as much as 1 L and still have little hemodynamic effect.5 Slowly developing effusions allow time for the pericardium to be compliant and stretch.

The pressures measured by hemodynamic catheters are increased because the increased intrapericardial pressures are exerting an effect on the heart chambers. While increased pericardial pressure decreases cardiac volume, the measured pressure is still increased. In any cardiac condition, the measured filling pressure only reflects true preload when the chamber compliance, the pericardial space, and pericardial layers are normal.5

The decreased stroke volume results in neurohormonal compensatory responses to maintain organ perfusion. Increased sympathetic stimulation results in catecholamine release and increased contractility, tachycardia, and vasoconstriction. Sinus tachycardia reflects exhaustion of compensatory mechanisms and signals not only the presence of a hemodynamically important effusion, but may be indicative of impending hemodynamic collapse.5

Figure 30-3 Mechanism of pulsus paradoxus.

Assessment Findings

A hemodynamically significant effusion may result in the symptoms of dyspnea, right heart failure, sinus tachycardia, and hypotension. Cardiac tamponade is a life-threatening condition that is diagnosed clinically by elevated jugular venous pressure, hypotension, and pulsus paradoxus in the setting of a pericardial effusion.3 Although cardiac tamponade increases filling pressures, cardiac volumes are reduced. Right and left heart filling pressures are increased and equalized, but the amount of fluid in the pulmonary veins is modest. Therefore, in cardiac tamponade, lungs are typically clear despite profound shortness of breath.5

Pulsus paradoxus is defined as an inspiratory decrease in systolic blood pressure greater than 10 mm Hg.5 Figure 30-3 depicts the mechanism of pulsus paradoxus as seen in pericardial tamponade.5 It is easily observed on arterial line tracings and can be detected by using a sphygmomanometer. To measure the blood pressure change using a blood pressure cuff, inflate the cuff to 15 mm Hg above the highest systolic reading. The cuff is slowly deflated until the first Korotkoff sounds are heard. The sounds are heard only with some heartbeats; these are the ones occurring during expiration at that pressure. The other sounds are heard at a lower pressure during inspiration. Slowly deflate the cuff until all of the Korotkoff sounds can be heard. The difference between these two readings gives the size of the pulsus.2

Medical Management

The treatment of pericardial tamponade is pericardiocentesis, drainage of the fluid accumulated in the pericardium by needle paracentesis.36 The use of echocardiographic imaging or fluoroscopy increases the safety and success of the procedure. Continuous hemodynamic monitoring of the effects of the procedure is critical. Surgery may be required if the cause of the tamponade is bleeding. A catheter can be placed for prolonged drainage.36

Nursing Management in Pericardial Disease

The nurse is perfectly positioned to recognize the symptoms of pericardial disease and the potential complications. The first priority of nursing management in pericardial disease is the recognition of the patient exhibiting hemodynamic compromise. It is critical that the patient maintain an adequate CO for organ perfusion. The nurse evaluates the patient’s hemodynamic state, evaluating vital signs, symptoms, presence of pulsus paradoxus, and jugular venous distension. The nurse implements interventions that improve cardiac function, including oxygen, vasoactive medications, fluid management, and decreasing anxiety and stress. Nurses monitor for cardiac arrhythmias and evaluate their effects on the patient’s condition. It is imperative that cardiac tamponade be diagnosed early, before hemodynamic collapse. Upon identification of a patient at risk, the nurse has the equipment readily available for an emergency pericardiocentesis. Close monitoring of the patient’s condition during and after the procedure reveals any other complications.

The nurse who is knowledgeable of pericardial disease is able to identify the patients most at risk, such as those with renal failure or recent MI. Evaluation of history, physical exam, laboratory results, ECGs, and vital signs are key nursing interventions that have an enormous impact on the patient’s outcome. A careful and skilled assessment is pivotal and points to the medical diagnosis of pericardial disease. To ensure appropriate treatment, the nurse needs to be aware of the subtle differences between symptoms of pericarditis and other conditions that cause chest pain, such as MI and pulmonary embolus. The characteristics of pericardial pain, including intermittent presence, location, quality, and the effect of position changes, are aspects of the patient’s condition that nurses are best suited to assess. Because a pericardial friction rub is likely to come and go, and change in quality, the nurse is most likely to find the sound as the member of the health care team who is consistently and frequently evaluating the patient.

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Jan 10, 2021 | Posted by in NURSING | Comments Off on Pericardial, Myocardial, and Endocardial Disease
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