Pericardial Disease
A. Acute pericarditis
1. Etiology
a. Myocardial infarction (MI). Pericarditis may occur in the first 24 hours following transmural MI because the inflamed surface of the infarcted area of myocardium produces pericardial irritation. A second type of pericarditis, called Dressler's syndrome, also may be seen from 1 week to several months after MI and may occur as the result of an autoimmune reaction to the damaged heart muscle.
b. Infection. Pericarditis frequently follows upper respiratory tract viral infections and is seen in many viral infections, including HIV, hepatitis, and many more. Tuberculosis, streptococcal infection, staphylococcal infection, and the sequelae of infective endocarditis also may produce pericarditis.
c. Collagen vascular disease. Acute pericarditis may be a clinical manifestation of SLE, rheumatoid arthritis, or, less commonly, scleroderma.
d. Drugs. Commonly used drugs that may cause acute pericarditis include procainamide, hydralazine, and isoniazid.
e. Malignancy. Pericarditis may occur secondary to metastatic involvement of the pericardium. Pulmonary and breast carcinomas are the most common primary sites.
f. Uremia. Pericarditis is common in untreated or undertreated severe chronic renal failure.
g. Postpericardiotomy syndrome. During open heart surgery, the pericardium is incised. Usually, the pericarditis that arises from this injury is short-lived; however, it may be protracted and severe in some patients.
h. Radiation. Radiation therapy delivered to the chest for thoracic malignancies may cause pericarditis.
2. Clinical features
a. Symptoms. The most common symptom in pericarditis is inspiratory chest pain.
(1) The pain is located in the left side and often is lessened when the patient sits up and leans forward.
(2) Occasionally the pain may be similar to that of myocardial ischemia and may radiate to the neck and arm.
b. Physical signs. The classic sign of acute pericarditis is the pericardial friction rub, which is a scratchy, leathery sound with three components corresponding to ventricular systole, early diastolic filling, and atrial contraction.
3. Diagnosis
a. Physical examination. The presence of a pericardial friction rub confirms the diagnosis of pericarditis.
b. Electrocardiography. Epicardial inflammation produces a diffuse current of injury with ST-segment elevation throughout the ECG. There is no reciprocal ST-segment depression, as is seen in acute MI. Depression of the PR segment is unique to pericarditis.
c. Echocardiography. The echocardiogram frequently demonstrates a pericardial effusion, which helps confirm the diagnosis.
4. Therapy
a. Specific therapy should be directed toward the cause of the pericarditis, if the cause is known.
b. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, indomethacin, and ibuprofen usually are effective in reducing the inflammation and relieving the chest pain.
c. Colchicine. Intractable cases of pericarditis, as may occur with Dressler's syndrome and postpericardiotomy syndrome, may require glucocorticoid therapy for relief of symptoms. Recently colchicine has replaced steroids at many centers.
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B. Pericardial effusion
1. Pathophysiology. The inflammation caused by acute pericarditis often produces exudation of fluid into the pericardial space. When fluid accumulates slowly, the pericardium expands to accommodate it, but when fluid accumulates rapidly, it compresses the heart, thus inhibiting cardiac filling. This latter condition is known as cardiac tamponade (see VI C).
2. Clinical features
a. Symptoms. The mere presence of a pericardial effusion does not cause symptoms. However, symptoms of acute pericarditis may coexist with a pericardial effusion.
b. Physical signs. As the effusion accumulates, it acts as a cushion around the heart.
(1) The precordium becomes quiet, palpation of the PMI becomes difficult, and the heart tones become distant and soft.
(2) Although the accumulation of fluid between the layers of pericardium may diminish a pericardial friction rub, a friction rub still may exist in the presence of a large effusion.
3. Diagnosis
a. Electrocardiography. The ECG demonstrates low voltage; electrical alternans may be present n large effusion.
b. Chest radiography. Cardiac enlargement occurs as the effusion develops. Typically, the cardiac silhouette has a “water bottle†appearance. The presence of an extremely enlarged heart without signs of vascular congestion suggests the diagnosis of pericardial effusion.
c. Echocardiography. An echocardiogram demonstrating an echo-free space between the two layers of the pericardium is diagnostic of a pericardial effusion.
d. Pericardiocentesis. The presence of a pericardial effusion may be confirmed by the aspiration of fluid from the pericardial sac. Examination of the fluid helps establish the cause of the effusion.
(1) The fluid should be sent for a cell count and differential, bacterial and fungal cultures, stains and cultures for Mycobacterium tuberculosis, protein content, and lactate dehydrogenase (LDH) content.
(2) An additional aliquot of fluid should be centrifuged and examined for tumor cells.
(3) Bloody effusions are characteristic of certain etiologies (e.g., neoplasia, tuberculosis). However, bloody effusions can also occur if the needle is passed too far and ventricular blood is aspirated by mistake. It is possible to distinguish the two because ventricular blood clots, whereas a bloody effusion does not.
e. Therapy. Treatment for a pericardial effusion is the same as that for acute pericarditis but may also involve aspiration.
C. Cardiac tamponade
1. Definition and pathophysiology. Cardiac tamponade is a life-threatening condition in which a pericardial effusion has developed so rapidly or has become so large that it compresses the heart.
a. The heart cannot fill adequately, and because the heart can pump out only what it takes in, impaired filling causes a profound reduction in cardiac output.
b. The external pressure produced by the fluid on the four chambers of the heart is dispersed equally. Because external pressure usually rises to a greater level than the normal cardiac filling pressures, intrapericardial pressure, left and right atrial pressures, and left and right ventricular pressures all become equal in diastole.
2. Clinical features
a. Symptoms. Most patients with cardiac tamponade complain of dyspnea, fatigue, and orthopnea.
b. Physical signs
(1) Pulsus paradoxus. The normal fall in systolic blood pressure that occurs during inspiration is exaggerated in tamponade. A decrease of more than 10 mm Hg occurs in 95% of patients with cardiac tamponade. The presence of pulsus paradoxus implies that stroke volume is falling during inspiration, probably as a result of the following mechanisms:
(a) Septal shift. During inspiration, right ventricular filling is augmented by negative intrathoracic pressure, which increases venous return. This causes transient enlargement of the right ventricle and pushes the ventricular septum into the left ventricle, thus reducing the size and output of the left ventricle.
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(b) Tensing of the pericardium. Inspiration produces downward traction on the pericardium, further compressing the cardiac structures and reducing left ventricular output.
(c) Right ventricular enlargement. The enhanced right ventricular filling during inspiration also distends the right ventricle, causing it to take up more room in the pericardial space. This further limits left ventricular filling.
(d) Negative intrathoracic pressure. During inspiration, the negative pressure inside the chest subtracts pressure from the extrathoracic vasculature, further reducing blood pressure.
(e) Expansion of the pulmonary vascular bed. The pulmonary vascular bed expands during inspiration, increasing its capacity and, thus, reduces left atrial filling.
(2) Neck vein distention. The intrapericardial pressure and right atrial pressure is reflected by extreme elevation of the jugular venous pressure. However, Kussmaul's sign (i.e., increased neck vein distention with inspiration) usually is absent in this condition.
(3) Narrowed pulse pressure. Reduction in left ventricular stroke volume leads to a reduction in systolic pressure; the tachycardia that usually occurs as a compensatory mechanism diminishes diastolic runoff and maintains diastolic pressure. Thus, pulse pressure is narrowed; however, less severe cases of cardiac tamponade may coexist with a normal pulse pressure.
(4) Shock. The carotid upstroke is diminished in volume, the systolic blood pressure is reduced, and the periphery is cold and clammy because of the vasoconstriction present in reduced cardiac output states.
3. Diagnosis. Elevated neck veins, pulsus paradoxus, and an enlarged cardiac silhouette on chest x-ray in a patient exhibiting symptoms of compromised cardiac output strongly suggest the diagnosis.
a. Echocardiography is an indispensable tool in the evaluation of tamponade. Features consistent with tamponade include:
(1) Presence of a pericardial effusion,
(2) Collapse of the right atrium and/or right ventricle, which occurs in diastole as the pericardial pressure exceeds the intracavitary pressure,
(3) Enhanced inspiratory trans-tricuspid flow and simultaneously reduced trans-mitral flow. This is the echo equivalent of a pulsus paradoxus.
b. Cardiac catheterization, which could confirm the diastolic equalization of pressures, is less commonly used for diagnosis of tamponade.
4. Therapy. The only effective therapy for cardiac tamponade is removal of fluid from the pericardial sac. Thus, emergency pericardiocentesis is indicated. The use of pressor agents and volume expansion is of limited benefit until pericardiocentesis can be performed.
D. Constrictive pericarditis
1. Definition. Constrictive pericarditis is the diffuse thickening of the pericardium in reaction to prior inflammation, which results in reduced distensibility of the cardiac chambers. Cardiac output is limited, and filling pressures are increased to match the external constrictive force placed on the heart by the pericardium.
2. Etiology. Most conditions that cause acute pericarditis may lead to chronic constrictive pericarditis.
3. Clinical features
a. Symptoms. The clinical picture typically is dominated by symptoms of right-sided failure rather than left-sided failure.
(1) Most patients with constrictive pericarditis complain of dyspnea on exertion as a result of limited cardiac output. Although approximately 50% of patients complain of orthopnea, paroxysmal nocturnal dyspnea is rare.
(2) Symptoms related to systemic venous hypertension frequently are reported and include ascites, edema, and jaundice.
b. Physical signs
(1) Jugular venous distention. The jugular veins are distended, indicating systemic venous hypertension. Neck vein distention increases with inspiration (Kussmaul's sign).
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(2) Heart sounds. The heart sounds are distant. Early in diastole, a pericardial knock may be heard, which falls in the same cadence as an S3 but is higher pitched and corresponds to early, abrupt cessation of ventricular filling.
(3) Other signs of systemic venous hypertension. Ascites, edema, hepatic tenderness, and hepatomegaly are frequently present. It is not uncommon for constriction to masquerade as end-stage liver disease.
4. Diagnosis
a. Electrocardiography. The ECG shows low voltage in the limb leads. Atrial arrhythmias are common.
b. Chest radiography reveals pericardial calcification in 50% of patients. This finding is seen as a radiopaque ring around the heart in the lateral view. The heart usually is normal in size, although cardiomegaly occasionally is noted.
c. Echocardiography. Although pericardial thickening often can be detected, reliable diagnosis of constrictive pericarditis by echocardiography is difficult. However, Doppler interrogation of the mitral valve usually demonstrates an abnormal decrease in flow during inspiration.
d. Magnetic resonance imaging (MRI) gated to the cardiac cycle is an imaging technique capable of measuring pericardial thickness.
e. Cardiac catheterization reveals equal pressures in the four cardiac chambers during diastole; in addition, all pressures usually are elevated.
5. Therapy. Surgical removal of the pericardium is curative. However, immediate relief of constrictive symptoms may not occur for up to 6 weeks after pericardiectomy.
A. Acute pericarditis
1. Etiology
a. Myocardial infarction (MI). Pericarditis may occur in the first 24 hours following transmural MI because the inflamed surface of the infarcted area of myocardium produces pericardial irritation. A second type of pericarditis, called Dressler's syndrome, also may be seen from 1 week to several months after MI and may occur as the result of an autoimmune reaction to the damaged heart muscle.
b. Infection. Pericarditis frequently follows upper respiratory tract viral infections and is seen in many viral infections, including HIV, hepatitis, and many more. Tuberculosis, streptococcal infection, staphylococcal infection, and the sequelae of infective endocarditis also may produce pericarditis.
c. Collagen vascular disease. Acute pericarditis may be a clinical manifestation of SLE, rheumatoid arthritis, or, less commonly, scleroderma.
d. Drugs. Commonly used drugs that may cause acute pericarditis include procainamide, hydralazine, and isoniazid.
e. Malignancy. Pericarditis may occur secondary to metastatic involvement of the pericardium. Pulmonary and breast carcinomas are the most common primary sites.
f. Uremia. Pericarditis is common in untreated or undertreated severe chronic renal failure.
g. Postpericardiotomy syndrome. During open heart surgery, the pericardium is incised. Usually, the pericarditis that arises from this injury is short-lived; however, it may be protracted and severe in some patients.
h. Radiation. Radiation therapy delivered to the chest for thoracic malignancies may cause pericarditis.
2. Clinical features
a. Symptoms. The most common symptom in pericarditis is inspiratory chest pain.
(1) The pain is located in the left side and often is lessened when the patient sits up and leans forward.
(2) Occasionally the pain may be similar to that of myocardial ischemia and may radiate to the neck and arm.
b. Physical signs. The classic sign of acute pericarditis is the pericardial friction rub, which is a scratchy, leathery sound with three components corresponding to ventricular systole, early diastolic filling, and atrial contraction.
3. Diagnosis
a. Physical examination. The presence of a pericardial friction rub confirms the diagnosis of pericarditis.
b. Electrocardiography. Epicardial inflammation produces a diffuse current of injury with ST-segment elevation throughout the ECG. There is no reciprocal ST-segment depression, as is seen in acute MI. Depression of the PR segment is unique to pericarditis.
c. Echocardiography. The echocardiogram frequently demonstrates a pericardial effusion, which helps confirm the diagnosis.
4. Therapy
a. Specific therapy should be directed toward the cause of the pericarditis, if the cause is known.
b. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, indomethacin, and ibuprofen usually are effective in reducing the inflammation and relieving the chest pain.
c. Colchicine. Intractable cases of pericarditis, as may occur with Dressler's syndrome and postpericardiotomy syndrome, may require glucocorticoid therapy for relief of symptoms. Recently colchicine has replaced steroids at many centers.
P.31
B. Pericardial effusion
1. Pathophysiology. The inflammation caused by acute pericarditis often produces exudation of fluid into the pericardial space. When fluid accumulates slowly, the pericardium expands to accommodate it, but when fluid accumulates rapidly, it compresses the heart, thus inhibiting cardiac filling. This latter condition is known as cardiac tamponade (see VI C).
2. Clinical features
a. Symptoms. The mere presence of a pericardial effusion does not cause symptoms. However, symptoms of acute pericarditis may coexist with a pericardial effusion.
b. Physical signs. As the effusion accumulates, it acts as a cushion around the heart.
(1) The precordium becomes quiet, palpation of the PMI becomes difficult, and the heart tones become distant and soft.
(2) Although the accumulation of fluid between the layers of pericardium may diminish a pericardial friction rub, a friction rub still may exist in the presence of a large effusion.
3. Diagnosis
a. Electrocardiography. The ECG demonstrates low voltage; electrical alternans may be present n large effusion.
b. Chest radiography. Cardiac enlargement occurs as the effusion develops. Typically, the cardiac silhouette has a “water bottle†appearance. The presence of an extremely enlarged heart without signs of vascular congestion suggests the diagnosis of pericardial effusion.
c. Echocardiography. An echocardiogram demonstrating an echo-free space between the two layers of the pericardium is diagnostic of a pericardial effusion.
d. Pericardiocentesis. The presence of a pericardial effusion may be confirmed by the aspiration of fluid from the pericardial sac. Examination of the fluid helps establish the cause of the effusion.
(1) The fluid should be sent for a cell count and differential, bacterial and fungal cultures, stains and cultures for Mycobacterium tuberculosis, protein content, and lactate dehydrogenase (LDH) content.
(2) An additional aliquot of fluid should be centrifuged and examined for tumor cells.
(3) Bloody effusions are characteristic of certain etiologies (e.g., neoplasia, tuberculosis). However, bloody effusions can also occur if the needle is passed too far and ventricular blood is aspirated by mistake. It is possible to distinguish the two because ventricular blood clots, whereas a bloody effusion does not.
e. Therapy. Treatment for a pericardial effusion is the same as that for acute pericarditis but may also involve aspiration.
C. Cardiac tamponade
1. Definition and pathophysiology. Cardiac tamponade is a life-threatening condition in which a pericardial effusion has developed so rapidly or has become so large that it compresses the heart.
a. The heart cannot fill adequately, and because the heart can pump out only what it takes in, impaired filling causes a profound reduction in cardiac output.
b. The external pressure produced by the fluid on the four chambers of the heart is dispersed equally. Because external pressure usually rises to a greater level than the normal cardiac filling pressures, intrapericardial pressure, left and right atrial pressures, and left and right ventricular pressures all become equal in diastole.
2. Clinical features
a. Symptoms. Most patients with cardiac tamponade complain of dyspnea, fatigue, and orthopnea.
b. Physical signs
(1) Pulsus paradoxus. The normal fall in systolic blood pressure that occurs during inspiration is exaggerated in tamponade. A decrease of more than 10 mm Hg occurs in 95% of patients with cardiac tamponade. The presence of pulsus paradoxus implies that stroke volume is falling during inspiration, probably as a result of the following mechanisms:
(a) Septal shift. During inspiration, right ventricular filling is augmented by negative intrathoracic pressure, which increases venous return. This causes transient enlargement of the right ventricle and pushes the ventricular septum into the left ventricle, thus reducing the size and output of the left ventricle.
P.32
(b) Tensing of the pericardium. Inspiration produces downward traction on the pericardium, further compressing the cardiac structures and reducing left ventricular output.
(c) Right ventricular enlargement. The enhanced right ventricular filling during inspiration also distends the right ventricle, causing it to take up more room in the pericardial space. This further limits left ventricular filling.
(d) Negative intrathoracic pressure. During inspiration, the negative pressure inside the chest subtracts pressure from the extrathoracic vasculature, further reducing blood pressure.
(e) Expansion of the pulmonary vascular bed. The pulmonary vascular bed expands during inspiration, increasing its capacity and, thus, reduces left atrial filling.
(2) Neck vein distention. The intrapericardial pressure and right atrial pressure is reflected by extreme elevation of the jugular venous pressure. However, Kussmaul's sign (i.e., increased neck vein distention with inspiration) usually is absent in this condition.
(3) Narrowed pulse pressure. Reduction in left ventricular stroke volume leads to a reduction in systolic pressure; the tachycardia that usually occurs as a compensatory mechanism diminishes diastolic runoff and maintains diastolic pressure. Thus, pulse pressure is narrowed; however, less severe cases of cardiac tamponade may coexist with a normal pulse pressure.
(4) Shock. The carotid upstroke is diminished in volume, the systolic blood pressure is reduced, and the periphery is cold and clammy because of the vasoconstriction present in reduced cardiac output states.
3. Diagnosis. Elevated neck veins, pulsus paradoxus, and an enlarged cardiac silhouette on chest x-ray in a patient exhibiting symptoms of compromised cardiac output strongly suggest the diagnosis.
a. Echocardiography is an indispensable tool in the evaluation of tamponade. Features consistent with tamponade include:
(1) Presence of a pericardial effusion,
(2) Collapse of the right atrium and/or right ventricle, which occurs in diastole as the pericardial pressure exceeds the intracavitary pressure,
(3) Enhanced inspiratory trans-tricuspid flow and simultaneously reduced trans-mitral flow. This is the echo equivalent of a pulsus paradoxus.
b. Cardiac catheterization, which could confirm the diastolic equalization of pressures, is less commonly used for diagnosis of tamponade.
4. Therapy. The only effective therapy for cardiac tamponade is removal of fluid from the pericardial sac. Thus, emergency pericardiocentesis is indicated. The use of pressor agents and volume expansion is of limited benefit until pericardiocentesis can be performed.
D. Constrictive pericarditis
1. Definition. Constrictive pericarditis is the diffuse thickening of the pericardium in reaction to prior inflammation, which results in reduced distensibility of the cardiac chambers. Cardiac output is limited, and filling pressures are increased to match the external constrictive force placed on the heart by the pericardium.
2. Etiology. Most conditions that cause acute pericarditis may lead to chronic constrictive pericarditis.
3. Clinical features
a. Symptoms. The clinical picture typically is dominated by symptoms of right-sided failure rather than left-sided failure.
(1) Most patients with constrictive pericarditis complain of dyspnea on exertion as a result of limited cardiac output. Although approximately 50% of patients complain of orthopnea, paroxysmal nocturnal dyspnea is rare.
(2) Symptoms related to systemic venous hypertension frequently are reported and include ascites, edema, and jaundice.
b. Physical signs
(1) Jugular venous distention. The jugular veins are distended, indicating systemic venous hypertension. Neck vein distention increases with inspiration (Kussmaul's sign).
P.33
(2) Heart sounds. The heart sounds are distant. Early in diastole, a pericardial knock may be heard, which falls in the same cadence as an S3 but is higher pitched and corresponds to early, abrupt cessation of ventricular filling.
(3) Other signs of systemic venous hypertension. Ascites, edema, hepatic tenderness, and hepatomegaly are frequently present. It is not uncommon for constriction to masquerade as end-stage liver disease.
4. Diagnosis
a. Electrocardiography. The ECG shows low voltage in the limb leads. Atrial arrhythmias are common.
b. Chest radiography reveals pericardial calcification in 50% of patients. This finding is seen as a radiopaque ring around the heart in the lateral view. The heart usually is normal in size, although cardiomegaly occasionally is noted.
c. Echocardiography. Although pericardial thickening often can be detected, reliable diagnosis of constrictive pericarditis by echocardiography is difficult. However, Doppler interrogation of the mitral valve usually demonstrates an abnormal decrease in flow during inspiration.
d. Magnetic resonance imaging (MRI) gated to the cardiac cycle is an imaging technique capable of measuring pericardial thickness.
e. Cardiac catheterization reveals equal pressures in the four cardiac chambers during diastole; in addition, all pressures usually are elevated.
5. Therapy. Surgical removal of the pericardium is curative. However, immediate relief of constrictive symptoms may not occur for up to 6 weeks after pericardiectomy.
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