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Pericardial Disease TABLE 31 . Causes of Pericardial Disease F \ Category lnfectious Viral infection Cause Enterovirus, herpesvirus, adenovirus, parvovirus Bacterial Myco b a cte ri u m tu be rcu I o si s, infection Pneu mococcu s spp., Staphy/ococcus spp Coxiel I a bu rnetii, Borre I a bu rgdo rfe ri i

Enterovirus, herpesvirus, adenovirus, parvovirus Bacterial Myco b a cte ri u m tu be rcu I o si s, infection Pneu mococcu s spp., Staphy/ococcus spp Coxiel I a bu rnetii, Borre I a bu rgdo rfe ri i Fungal infeaion H i sto p I a sm a, Aspe rg i I I u s, B I a stomyce s, Candida spp. Noninfectious Autoimmune Systemic lupus erythematosus, diseases rheumatoid arthritis, Sjogren syndrome, systemic sclerosis, sarcoidosis, familial Mediterranean fever Cance Metastatic lung cancer, breast cancer, and melanoma; lymphoma and leukemia Metabolic Uremia, myxedema F I G UR E 4 1 . Cardiac magnetic resonance image in a patient with an angiosarcoma. conditions A heterogeneous m asslwhite anow)isinfiltrating the right atrial wall. A pericard ial Drug-related Hydralazine, procainamide, minoxidil, eflusion(yellow arrow) is also present. causes all-trans retinoic acid latrogenic causes Cardiac surgery (postpericardiotomy from a right atrial mlxoma. Most patients die in 6 to 12 months. syndrome), coronary perforation during Even when complete surgical extirpation is possible, survival percutaneous intervention, pacemaker remains less than 2 years for most patients. lead penetration, radiofrequency ablation Other lrradiation, aortic dissection, pulmonary r(EY P0rt{Ts arterial hypertension . An atrial myxoma should be considered in patients with auscultatory findings of mitral stenosis that vary with position. sound classically has three components corresponding to the . Atrial myxomas should be surgically removed to prevent cardiac rycle during norrnal sinus rhythm: atrial systole. \,en-

Fungal infeaion H i sto p I a sm a, Aspe rg i I I u s, B I a stomyce s, Candida spp. Noninfectious Autoimmune Systemic lupus erythematosus, diseases rheumatoid arthritis, Sjogren syndrome, systemic sclerosis, sarcoidosis, familial Mediterranean fever Cance Metastatic lung cancer, breast cancer, and melanoma; lymphoma and leukemia Metabolic Uremia, myxedema F I G UR E 4 1 . Cardiac magnetic resonance image in a patient with an angiosarcoma. conditions A heterogeneous m asslwhite anow)isinfiltrating the right atrial wall. A pericard ial Drug-related Hydralazine, procainamide, minoxidil, eflusion(yellow arrow) is also present. causes all-trans retinoic acid latrogenic causes Cardiac surgery (postpericardiotomy from a right atrial mlxoma. Most patients die in 6 to 12 months. syndrome), coronary perforation during Even when complete surgical extirpation is possible, survival percutaneous intervention, pacemaker remains less than 2 years for most patients. lead penetration, radiofrequency ablation Other lrradiation, aortic dissection, pulmonary r(EY P0rt{Ts arterial hypertension . An atrial myxoma should be considered in patients with auscultatory findings of mitral stenosis that vary with position. sound classically has three components corresponding to the . Atrial myxomas should be surgically removed to prevent cardiac rycle during norrnal sinus rhythm: atrial systole. \,en- embolic events. tricular systole, and ventricular filling. The three phases ofthe pericardial friction rub differentiate it from a pleural friction rub, which has two components linked to respiration. Less commonly, the rub of pericarditis may be monophasic or bipha Pericardial Disease sic, but it is not affected by respiration. Auscultation should be performed during end expiration n ith the patient in the supine Acute Pericarditis position or sifting upright. Clinical Presentation and Evaluation The tlpical ECG feature of acute pericarditis is concave Pericarditis is inflammation of the pericardium, the thin ST-segment elevation in multiple leads that does not corre fibrous sac surrounding the heart. It may be subclinical or spond with a single coronary artery distribution. PR segment present as sharp precordial pain of acute onset. Acute pericar- depression in lead II or reciprocal PR segment eler'ation in ditis has many causes (Table 31), but it is most often idiopathic lead aVR also may be present (Figure 42). In contrast. ECG or presumed viral in origin. findings of acute myocardial infarction are hyperacute T Acute pericarditis is diagnosed clinically by the presence waves, ST-segment elevation consistent with a single coronary of at least two of four criteria: chest pain typical for pericardi- distribution, reciprocal ST-segment depression, pathologic Q tis, a pericardial friction rub, new ECG changes, or a new peri- waves during myocardial infarction evolution, and absence of cardial effusion (Table 32). Chest pain attributable to acute PR-segment change. pericarditis is typically sharp, severe, and positional. It is not Echocardiography should be performed to evaluate fbr exacerbated by exertion nor relieved by rest or nitrogfcerin, pericardial effusion; however, the absence of effusion does not unlike anginal pain. Pain is characteristically worse in the exclude acute pericarditis. When the diagnosis remains uncer supine position and improves with sitting up and leaning tain, cardiac magnetic resonance (CMR) imaging u'ith intrave forward. These pain features may be related to tension of the nous gadolinium contrast may be used to identifi'evidence of pericardium at its sternal and diaphragmatic attachments. pericardial inflammation, characterized by pericardial thicken A pericardial friction rub is a hallmark of acute pericarditis ing and late gadolinium enhancement (Figure 43). Alternatively, and is frequently present on auscultation. The harsh, scratchy gated cardiac CT may demonstrate pericardial inflammation.

embolic events. tricular systole, and ventricular filling. The three phases ofthe pericardial friction rub differentiate it from a pleural friction rub, which has two components linked to respiration. Less commonly, the rub of pericarditis may be monophasic or bipha Pericardial Disease sic, but it is not affected by respiration. Auscultation should be performed during end expiration n ith the patient in the supine Acute Pericarditis position or sifting upright. Clinical Presentation and Evaluation The tlpical ECG feature of acute pericarditis is concave Pericarditis is inflammation of the pericardium, the thin ST-segment elevation in multiple leads that does not corre fibrous sac surrounding the heart. It may be subclinical or spond with a single coronary artery distribution. PR segment present as sharp precordial pain of acute onset. Acute pericar- depression in lead II or reciprocal PR segment eler'ation in ditis has many causes (Table 31), but it is most often idiopathic lead aVR also may be present (Figure 42). In contrast. ECG or presumed viral in origin. findings of acute myocardial infarction are hyperacute T Acute pericarditis is diagnosed clinically by the presence waves, ST-segment elevation consistent with a single coronary of at least two of four criteria: chest pain typical for pericardi- distribution, reciprocal ST-segment depression, pathologic Q tis, a pericardial friction rub, new ECG changes, or a new peri- waves during myocardial infarction evolution, and absence of cardial effusion (Table 32). Chest pain attributable to acute PR-segment change. pericarditis is typically sharp, severe, and positional. It is not Echocardiography should be performed to evaluate fbr exacerbated by exertion nor relieved by rest or nitrogfcerin, pericardial effusion; however, the absence of effusion does not unlike anginal pain. Pain is characteristically worse in the exclude acute pericarditis. When the diagnosis remains uncer supine position and improves with sitting up and leaning tain, cardiac magnetic resonance (CMR) imaging u'ith intrave forward. These pain features may be related to tension of the nous gadolinium contrast may be used to identifi'evidence of pericardium at its sternal and diaphragmatic attachments. pericardial inflammation, characterized by pericardial thicken A pericardial friction rub is a hallmark of acute pericarditis ing and late gadolinium enhancement (Figure 43). Alternatively, and is frequently present on auscultation. The harsh, scratchy gated cardiac CT may demonstrate pericardial inflammation. 84

I ! l Pericardial Disease 3 t TABLE 32. Evaluation of Pericardial Disease Evaluation Acute Pericarditis Cardiac Tamponade Constrictive Pericarditis I Physical Three-component friction rub Tachycardia, elevated CVB Elevated CVP, increasing CVP with examination diminished y descent, pulsus inspiration, pericardial knock, right- paradoxus, pericardial rub if sided HF inflammatory etiology I ECG Concave ST-seg ment elevation Sinus tachycardia, electrical No pathognomonic findings in multiple leads, PR-segment alternans, possible low voltage depression in lead ll or PR-segment elevation in aVR Chest radiography Usually normal Possible enlarged cardiac silhouette Possible pericardial calcification, (water bottle heart), clear lungs more often normal Echoca rd iog raphy Possible pericardial effusion RV early diastolic collapse, RA late lncreased pericardial thickness, diastolic collapse, abnormal inspiratory decrease in mitral inflow t interventricular septal motion, velocity, biatrial enlargement, normal inspiratory decrease in mitral inflow ventricular size and systolic function, velocity, IVC plethora IVC plethora t- CMR imaging Pericardial inflammation with Usually not necessary Pericardial thickening and i late gadolinium enhancement calcification CT Pericard ial inflammation Usually not necessary Pericardial thickening and t ca lcification

t TABLE 32. Evaluation of Pericardial Disease Evaluation Acute Pericarditis Cardiac Tamponade Constrictive Pericarditis I Physical Three-component friction rub Tachycardia, elevated CVB Elevated CVP, increasing CVP with examination diminished y descent, pulsus inspiration, pericardial knock, right- paradoxus, pericardial rub if sided HF inflammatory etiology I ECG Concave ST-seg ment elevation Sinus tachycardia, electrical No pathognomonic findings in multiple leads, PR-segment alternans, possible low voltage depression in lead ll or PR-segment elevation in aVR Chest radiography Usually normal Possible enlarged cardiac silhouette Possible pericardial calcification, (water bottle heart), clear lungs more often normal Echoca rd iog raphy Possible pericardial effusion RV early diastolic collapse, RA late lncreased pericardial thickness, diastolic collapse, abnormal inspiratory decrease in mitral inflow t interventricular septal motion, velocity, biatrial enlargement, normal inspiratory decrease in mitral inflow ventricular size and systolic function, velocity, IVC plethora IVC plethora t- CMR imaging Pericardial inflammation with Usually not necessary Pericardial thickening and i late gadolinium enhancement calcification CT Pericard ial inflammation Usually not necessary Pericardial thickening and t ca lcification Cardiac Not applicable Usually not necessary Ventricular interdependence, square catheterization root signs in RV and LV pressure tracings ,- CMR= cardiac magnetic resonance; CVP=central venous pressure; HF = heartfailure; IVC = nferlorvena cava; LV= eftventric!lar; RA= right atrial; RV= right ventricular

Cardiac Not applicable Usually not necessary Ventricular interdependence, square catheterization root signs in RV and LV pressure tracings ,- CMR= cardiac magnetic resonance; CVP=central venous pressure; HF = heartfailure; IVC = nferlorvena cava; LV= eftventric!lar; RA= right atrial; RV= right ventricular a '1 Additional findings that support acute pericarditis include Although most cases of acute pericarditis are idiopathic fever and serologic evidence of inflammation (leukocl,tosis, or viral, a search fbr alternative causes is appropriate (see elevated erythrocyte sedimentation rate or C-reactive protein Table 31). Additional testing beyond the initial evaluation is [CRP] lerel). Serum cardiac troponin levels are normal or may based on suspicion for a specific cause. Tuberculosis should be be slightly elevated if there is a component of myopericarditis. considered in hospital workers, persons who are incarcerated I ; { FIGURE 42. ECGchangesofacutepericarditis.ConcaveST-segmentelevationispresentinmostoftheleads(arowheads).ThePRsegmentisdepressedinallleadsexcept aVR (arrows). 85

Pericardial Disease I tapering. CRP may be useful as a marker of treatment response, l with tapering initiated after the CRP level normalizes. Glucocorticoid therapy is reserved for patients with per- t i icarditis that is recurrent, incessant (>4 6 u,eeks'duration). '! or chronic (>3 months' duration) despite standard therapy: i uremic pericarditis not responsive to intensive dialysis; con I i traindications to NSAID therapy; or autoimmune-mediated pericarditis. Prednisone is added to standard therapl, (aspi I

uremic pericarditis not responsive to intensive dialysis; con I i traindications to NSAID therapy; or autoimmune-mediated pericarditis. Prednisone is added to standard therapl, (aspi I riniNSAIDs and colchicine) at a dosage of 0.25 mg,'kg to 0.5 mg/kg and continued for 3 months. Tapering should not I be initiated until after the first 2 to 4 weeks of therapy or until i the CRP level normalizes. Targeted inhibition of interleukin I with rilonacept is an effective glucocorticoid sparing therapy fbr idiopathic recurrent pericarditis refractory to standard treatment. Expert consensus opinion is that athletes should not return to competitive exercise for 3 months from initial onset ofpericarditis and that nonathletes restrict strenuous activity until symptoms resolve. xtY Potilrs F I G UR E 4 3. Cardiac magnetic resonance image obtained after intravenous o Acute pericarditis is diagnosed by the presence ofat administration of gadolinium. A pericardial effusion ( red anow\ is present, and there is late gadolinium enhancement of the pericardium consistent with least tvvo offour criteria: chest pain typical for pericar inflam mation (white a rrowl. ditis, a pericardial friction rub, new ECG changes. or a new pericardial effusion. or residing in chronic care facilities, and residents ofor travel o First line therapy for acute idiopathic pericarditis is ers to an endemic area. Treatment of tuberculosis may reduce high dose aspirin or NSAIDs and adjuvant colchicine the risk for reactive pericardial constriction from greater therapy. than B0'1, to less than 10'){,. Other causes of acute pericarditis o Glucocorticoid therapy is reserved for patients with include uremia, recent cardiac surgery. and chest irradiation. incessant, recurrent, or chronic pericarditis despite Postpericardiotomy syndrome, characterized by pericardial standard therapy; uremic pericarditis not responsive to inflammation that is likely autoimmune in nature, may occur : intensive dialysis; contraindications to NSAID therapy; after cardiac surgery with a latency period of several weeks. or autoimmune-mediated pericarditis. The presentation and treatment of postpericardiotomy syn drome are similar to those ol idiopathic pericarditis.

riniNSAIDs and colchicine) at a dosage of 0.25 mg,'kg to 0.5 mg/kg and continued for 3 months. Tapering should not I be initiated until after the first 2 to 4 weeks of therapy or until i the CRP level normalizes. Targeted inhibition of interleukin I with rilonacept is an effective glucocorticoid sparing therapy fbr idiopathic recurrent pericarditis refractory to standard treatment. Expert consensus opinion is that athletes should not return to competitive exercise for 3 months from initial onset ofpericarditis and that nonathletes restrict strenuous activity until symptoms resolve. xtY Potilrs F I G UR E 4 3. Cardiac magnetic resonance image obtained after intravenous o Acute pericarditis is diagnosed by the presence ofat administration of gadolinium. A pericardial effusion ( red anow\ is present, and there is late gadolinium enhancement of the pericardium consistent with least tvvo offour criteria: chest pain typical for pericar inflam mation (white a rrowl. ditis, a pericardial friction rub, new ECG changes. or a new pericardial effusion. or residing in chronic care facilities, and residents ofor travel o First line therapy for acute idiopathic pericarditis is ers to an endemic area. Treatment of tuberculosis may reduce high dose aspirin or NSAIDs and adjuvant colchicine the risk for reactive pericardial constriction from greater therapy. than B0'1, to less than 10'){,. Other causes of acute pericarditis o Glucocorticoid therapy is reserved for patients with include uremia, recent cardiac surgery. and chest irradiation. incessant, recurrent, or chronic pericarditis despite Postpericardiotomy syndrome, characterized by pericardial standard therapy; uremic pericarditis not responsive to inflammation that is likely autoimmune in nature, may occur : intensive dialysis; contraindications to NSAID therapy; after cardiac surgery with a latency period of several weeks. or autoimmune-mediated pericarditis. The presentation and treatment of postpericardiotomy syn drome are similar to those ol idiopathic pericarditis. Management Pericardial Effusion and Most patients with acute pericarditis can be managed as out Cardiac Tamponade patients; however, patients with accompanying high risk Pericardial Effusion features may require hospitalization for treatment and moni Pericardial effusions are often asymptomatic, with incidental t toring. These predictors of poor prognosis include tempera discovery on chest radiograph, CT. or echocardiogram. ln ture higher than 38'C (100.4 "F), subacute onset (days to asymptomatic patients, most effusions are idiopathic: how weeks without acute chest pain at onset), a large pericardial ever, malignancy, infections, autoimmune disease. hlpothy effusion (>20 mm diastolic echo-free space) or tamponade at roidism, and iatrogenic causes (medications, anticoagulation : presentation, oral anticoagulation therapy, or lack ofresponse therapy) should be considered (see Table 31). ln countries (no relief in symptoms and/or inflammatory markers) after where tuberculosis is endemic. more than 60'/. of effusions are 1 week of treatment. caused by tuberculosis. First line therapy for acute idiopathic pericarditis is Pericardiocentesis should be considered for diagnostic aspirin (750 1000 mg) or NSAIDs (ibuprofen 600 mg) every and therapeutic purposes if cancer or bacterial infection is B hours for 1to 2 weeks. Colchicine (0.5 mg once or twice daily strongly suspected. In patients with pericardial effusion of ; ; for 3 months) is recommended as adjunctive therapy to unknown cause and elevated inflammatory markers. empiric shorten symptom duration and reduce treatment failure and treatment of pericarditis may be reasonable. Drainage should recurrence. Patients who respond to therapy initially but be considered for large idiopathic effusions ol more than develop recurrent pericarditis after treatment completion may 3 months' duration, because one in three patients progress to benefit from a longer course of standard therapy with slow cardiac tamponade.

Management Pericardial Effusion and Most patients with acute pericarditis can be managed as out Cardiac Tamponade patients; however, patients with accompanying high risk Pericardial Effusion features may require hospitalization for treatment and moni Pericardial effusions are often asymptomatic, with incidental t toring. These predictors of poor prognosis include tempera discovery on chest radiograph, CT. or echocardiogram. ln ture higher than 38'C (100.4 "F), subacute onset (days to asymptomatic patients, most effusions are idiopathic: how weeks without acute chest pain at onset), a large pericardial ever, malignancy, infections, autoimmune disease. hlpothy effusion (>20 mm diastolic echo-free space) or tamponade at roidism, and iatrogenic causes (medications, anticoagulation : presentation, oral anticoagulation therapy, or lack ofresponse therapy) should be considered (see Table 31). ln countries (no relief in symptoms and/or inflammatory markers) after where tuberculosis is endemic. more than 60'/. of effusions are 1 week of treatment. caused by tuberculosis. First line therapy for acute idiopathic pericarditis is Pericardiocentesis should be considered for diagnostic aspirin (750 1000 mg) or NSAIDs (ibuprofen 600 mg) every and therapeutic purposes if cancer or bacterial infection is B hours for 1to 2 weeks. Colchicine (0.5 mg once or twice daily strongly suspected. In patients with pericardial effusion of ; ; for 3 months) is recommended as adjunctive therapy to unknown cause and elevated inflammatory markers. empiric shorten symptom duration and reduce treatment failure and treatment of pericarditis may be reasonable. Drainage should recurrence. Patients who respond to therapy initially but be considered for large idiopathic effusions ol more than develop recurrent pericarditis after treatment completion may 3 months' duration, because one in three patients progress to benefit from a longer course of standard therapy with slow cardiac tamponade. 85

Pericardial Disease n v4 tt tt aVL 1 I v5 tt ltt iln v0 "1" VI I t- I Itt .l_, l^ ) l-, _l-, ^l^, l-, J l^ ^ l_ ^l^ n V5 FIGURE 44. ECGdemonstratingelectrical alternans,acyclicbeat-to-beatshiftinthe0RSaxisthatmayrepresentswingingof theheartwithinalargepericardial effusion, as well as supraventricular tachycardia.

Itt .l_, l^ ) l-, _l-, ^l^, l-, J l^ ^ l_ ^l^ n V5 FIGURE 44. ECGdemonstratingelectrical alternans,acyclicbeat-to-beatshiftinthe0RSaxisthatmayrepresentswingingof theheartwithinalargepericardial effusion, as well as supraventricular tachycardia. Cardiac Tamponade low voltage. If fluid has accumulated slowly, the cardiac sil Clinical Presentation and Evaluation houette is typically enlarged on chest radiograph (Figure 45). Cardiac tamponade occurs when tluid accumulation within Echocardiography is an essential tool in the diagnosis of the pericardial space compresses the heart and impedes dia- cardiac tamponade because it defines the presence, distribu- stolic filling. With rapid fluid accumulation, as may occur tion, and relative volume of pericarditrl fluid (Figure 46). Early with trauma, aortic dissection, or invasive cardiac procedures, diastolic collapse ofthe right ventricle, late diastolic collapse of' tamponade may arise at relatively low pericardial volumes. the right atrium, and abnormal interventricular septal motion Subacute or chronic processes, such as neoplastic disease or are echocardiographic I'eatures associated with cardiac tam hypothyroidism, may be associated with much larger efl'u- ponade. Doppler evaluation may additionally demonstrate a sions (several hundred milliliters in volume). decrease in mitral intlow velocity of more than 25'1, with Clinical signs o1'tamponade include tachycardia, muffled heart sounds, and elevated central venous pressure (see Table 32). Blood pressure may be elevated or normal early in the course due to adrenergic response, with ensuing hypoten- sion as intrapericardial pressures rise. 'l'he y descent of the jugular venous pulse may be absent because passive filling of' the ventricles is impeded by the intrapericardial pressure. This finding may be difficult to appreciate, especially in patients with tachycardia. Pulsus paradoxus represents exaggerated ven tricular interdependence and is a key clinical feature ofcardiac tamponade. It is characterized by a tall in systolic pressure o1 greater than 10 mm Hg during inspiration. Pulsus paradoxus is not specific for tamponade and must be interpreted in conjunc- tion with other clinicai and echocardiographic findings. The ECG in patients with tamponade may demonstrate sinus tachycardia, electrical alternans (related to a swinging FIGURE 45. Chest radiograph demonstrating an enlarged cardiacsilhouette motion of the heart within the pericardial Iluid) (Figure 44), or ("water bottle heart") in cardiac tamponade.

Cardiac Tamponade low voltage. If fluid has accumulated slowly, the cardiac sil Clinical Presentation and Evaluation houette is typically enlarged on chest radiograph (Figure 45). Cardiac tamponade occurs when tluid accumulation within Echocardiography is an essential tool in the diagnosis of the pericardial space compresses the heart and impedes dia- cardiac tamponade because it defines the presence, distribu- stolic filling. With rapid fluid accumulation, as may occur tion, and relative volume of pericarditrl fluid (Figure 46). Early with trauma, aortic dissection, or invasive cardiac procedures, diastolic collapse ofthe right ventricle, late diastolic collapse of' tamponade may arise at relatively low pericardial volumes. the right atrium, and abnormal interventricular septal motion Subacute or chronic processes, such as neoplastic disease or are echocardiographic I'eatures associated with cardiac tam hypothyroidism, may be associated with much larger efl'u- ponade. Doppler evaluation may additionally demonstrate a sions (several hundred milliliters in volume). decrease in mitral intlow velocity of more than 25'1, with Clinical signs o1'tamponade include tachycardia, muffled heart sounds, and elevated central venous pressure (see Table 32). Blood pressure may be elevated or normal early in the course due to adrenergic response, with ensuing hypoten- sion as intrapericardial pressures rise. 'l'he y descent of the jugular venous pulse may be absent because passive filling of' the ventricles is impeded by the intrapericardial pressure. This finding may be difficult to appreciate, especially in patients with tachycardia. Pulsus paradoxus represents exaggerated ven tricular interdependence and is a key clinical feature ofcardiac tamponade. It is characterized by a tall in systolic pressure o1 greater than 10 mm Hg during inspiration. Pulsus paradoxus is not specific for tamponade and must be interpreted in conjunc- tion with other clinicai and echocardiographic findings. The ECG in patients with tamponade may demonstrate sinus tachycardia, electrical alternans (related to a swinging FIGURE 45. Chest radiograph demonstrating an enlarged cardiacsilhouette motion of the heart within the pericardial Iluid) (Figure 44), or ("water bottle heart") in cardiac tamponade. 87

t I n I Pericardial Disease i I l i I I 1 i 1 I' I I ; i cardiac tamponade lrightpanel). LA= left atrium; LV= left ventricle; RA = right atrium; RV= right ventricle

I ; i cardiac tamponade lrightpanel). LA= left atrium; LV= left ventricle; RA = right atrium; RV= right ventricle inspiration, which is the echocardiographic equivalent of recurrent pericardial effusion by creating a pericardial u'in- pulsus paradoxus (Figure 47). dow (often used in cases of malignant pericardial effusion). Cardiac catheterization is rarely necessary for diagnosis. In hemodynamically unstable patients, intravenous normal Hemodynamic hallmarks of tamponade include blunting or saline is used to stabilize the patient as a temporizing meas loss of the U descent within the right atrial pressure waveform ure or bridge to definitive therapy. and elevated and equalized diastolic pressures. The latter reflects After pericardial drainage, hemodynamic and clinical the transmilted effect of the intrapericardial pressure. Invasive evaluation may occasionally disclose findings of underlying arterial pressure recordings also show pulsus paradoxus. pericardial constriction, termed eflusive constrictive pericar- 'l I ditis. If clinical evaluation and imaging studies (such as CMR , Management imaging) suggest an active inflammatory process. medical Cardiac tamponade is life-threatening, and urgent pericar therapy for acute pericarditis may be considered. with surgery dial drainage is required after diagnostic confirmation. reserved for refractory cases. Fluid removal can be accomplished r,r,ith pericardiocentesis l I(EY POITIS or a surgical subxiphoid approach. Pericardiocentesis is o Clinical features of cardiac tamponade include tachy- often performed using echocardiographic or fluoroscopic I

inspiration, which is the echocardiographic equivalent of recurrent pericardial effusion by creating a pericardial u'in- pulsus paradoxus (Figure 47). dow (often used in cases of malignant pericardial effusion). Cardiac catheterization is rarely necessary for diagnosis. In hemodynamically unstable patients, intravenous normal Hemodynamic hallmarks of tamponade include blunting or saline is used to stabilize the patient as a temporizing meas loss of the U descent within the right atrial pressure waveform ure or bridge to definitive therapy. and elevated and equalized diastolic pressures. The latter reflects After pericardial drainage, hemodynamic and clinical the transmilted effect of the intrapericardial pressure. Invasive evaluation may occasionally disclose findings of underlying arterial pressure recordings also show pulsus paradoxus. pericardial constriction, termed eflusive constrictive pericar- 'l I ditis. If clinical evaluation and imaging studies (such as CMR , Management imaging) suggest an active inflammatory process. medical Cardiac tamponade is life-threatening, and urgent pericar therapy for acute pericarditis may be considered. with surgery dial drainage is required after diagnostic confirmation. reserved for refractory cases. Fluid removal can be accomplished r,r,ith pericardiocentesis l I(EY POITIS or a surgical subxiphoid approach. Pericardiocentesis is o Clinical features of cardiac tamponade include tachy- often performed using echocardiographic or fluoroscopic I guidance. Surgical therapy is indicated to drain fluid when cardia, hypotension, muffled heart sounds, elevated I pericardiocentesis cannot be performed safely, to obtain central venous pressure, and pulsus paradoxus. pericardial tissue for diagnostic purposes, or to prevent o Cardiac tamponade requires urgent drainage of pericar i

guidance. Surgical therapy is indicated to drain fluid when cardia, hypotension, muffled heart sounds, elevated I pericardiocentesis cannot be performed safely, to obtain central venous pressure, and pulsus paradoxus. pericardial tissue for diagnostic purposes, or to prevent o Cardiac tamponade requires urgent drainage of pericar i dial fluid with either pericardiocentesis or surgery. I FR 29Hz 0 Constrictive Perica rditis 20 .t i! 5 10 t Clinical Presentation and Evaluation i Constrictive pericarditis is characterized by pericardial thick a 15

10 t Clinical Presentation and Evaluation i Constrictive pericarditis is characterized by pericardial thick a 15 ?0 ening, fibrosis. and sometimes calcification that impair dia ?5 stolic filling and limit total cardiac volume. Within developed 1 Ittspiration Expiration 1?A countries, most cases are idiopathic. Other causes include 80 cardiac surgery chest irradiation, autoimmune disease. and tuberculosis or other bacterial inf'ection. Tuberculosis remains l0 a major cause of constrictive pericarditis in developing I I l'*,,* lu ,[ ,t ,l l-i'l dt.r..l I I li l,p l$ 't, i* I * r..r flr, l? r& lr tr l[ Il;-"" countries. 't I Constrictive pericarditis most commonly presents as indo i - {u lent progression of right-sided heart failure symptoms. includ I

?0 ening, fibrosis. and sometimes calcification that impair dia ?5 stolic filling and limit total cardiac volume. Within developed 1 Ittspiration Expiration 1?A countries, most cases are idiopathic. Other causes include 80 cardiac surgery chest irradiation, autoimmune disease. and tuberculosis or other bacterial inf'ection. Tuberculosis remains l0 a major cause of constrictive pericarditis in developing I I l'*,,* lu ,[ ,t ,l l-i'l dt.r..l I I li l,p l$ 't, i* I * r..r flr, l? r& lr tr l[ Il;-"" countries. 't I Constrictive pericarditis most commonly presents as indo i - {u lent progression of right-sided heart failure symptoms. includ I ing peripheral edema and abdominal sr.relling (see Table 32). ) ,-4, 'r, FIGURE 47. Pulsed-waveDopplerevaluationofmitralinflowvelocity.Achangein Exertional dyspnea and fatigue are caused by increased dia- the flow between expiration and inspiration of greater than 250/o is present, consistent stolic pressures and limited ability to augment cardiac output with enhanced ventricular interdependence. due to the fixed stroke volume.

ing peripheral edema and abdominal sr.relling (see Table 32). ) ,-4, 'r, FIGURE 47. Pulsed-waveDopplerevaluationofmitralinflowvelocity.Achangein Exertional dyspnea and fatigue are caused by increased dia- the flow between expiration and inspiration of greater than 250/o is present, consistent stolic pressures and limited ability to augment cardiac output with enhanced ventricular interdependence. due to the fixed stroke volume. 88

Pericardial Disease On physical examination, the central venous pressure is TABLE 33. Characteristics of the Selected Diastolic elevated in nearly all patients, with prominent x and y Heart Sounds descents. The height of the waveform does not fall or may Diastolic Condition Characteristics increase during inspiration (Kussmaul sign), reflecting the Heart Sound fixed diastolic volume of the right heart. Early diastolic filling Opening snap Mitral High frequency is unimpaired or even accentuated and is followed by sudden stenosis Heard best at the left lower cessation when total acceptable volume is met, resulting in a sternal border and the apex high-frequency early diastolic sound (the pericardial knock). Associated with a loud S1, a Characteristics that may be used to differentiate a pericardial loud P2 with associated knock from other diastolic sounds are listed in Table 33. Pulsus pulmonary hypertension, and a low-pitched diastolic paradoxus is less frequent in constrictive pericarditis than in rumble at the apex cardiac tamponade. Peripheral edema, ascites, hepatomegaly, Pericardial Constrictive High frequency and pleural effusions are common. Muscle wasting may be knock pericarditis Heard throughout the evident in advanced cases. precordium An ECG is obtained as part of the initial evaluation and Earlierthan an 53 may reveal low voltage; however, no ECG findings are specific to constrictive pericarditis. Associated with deep x and y descents in the jugular Diagnosis of constrictive pericarditis is made with imaging venous pulse waveform studies and hemodynamic evaluation. Transthoracic echocar- Tumor plop Atrial Low frequency diography reveals normal right and left ventricular size and myxoma Heard best at the apex systolic function despite prominent symptoms and findings suggestive of heart failure. Dilatation ofthe inferior vena cava May be positional reflects elevated right-sided filling (right atrial) pressure. Dop- s3 Heart failure Low frequency pler echocardiography and tissue Doppler velocity are required Heard best at the apex and to differentiate constrictive pericarditis from restrictive cardio- the left lateral decubitus position myopathy (see Myocardial Disease). Myocardial relaxation is unimpaired or even enhanced in constrictive pericarditis, in Displaced point of maximal impulse which early diastolic filling is rapid and unimpeded, whereas relaxation is impaired in restrictive cardiomyopathy. Chest radiography or CT in constrictive pericarditis may Cardiac catheterization can be performed when con demonstrate partial or circumferential pericardial calcification strictive pericarditis is suspected but not confirmed by (Figure aS), and pericardial thickening (>3 mm) may be visible echocardiography. Invasive hemodynamic findings of con- on CT or CMR imaging. Importantly, constriction may exist in strictive pericarditis include a prominent y descent in the the absence of these findings. In one case series, hemody- right atrial waveform, which corresponds with the dip of namically proven constrictive pericarditis occurred with nor the right ventricular dip and plateau waveform (square mal pericardial thickness in 18% of cases. CMR imaging also root sign). The significant U descent and the right ventricu may demonstrate an inspiratory septal shift, a sign of ventricu- lar dip both represent unimpeded or rapid early diastolic lar interdependence. ventricular filling. As inflow volume reaches the fixed

On physical examination, the central venous pressure is TABLE 33. Characteristics of the Selected Diastolic elevated in nearly all patients, with prominent x and y Heart Sounds descents. The height of the waveform does not fall or may Diastolic Condition Characteristics increase during inspiration (Kussmaul sign), reflecting the Heart Sound fixed diastolic volume of the right heart. Early diastolic filling Opening snap Mitral High frequency is unimpaired or even accentuated and is followed by sudden stenosis Heard best at the left lower cessation when total acceptable volume is met, resulting in a sternal border and the apex high-frequency early diastolic sound (the pericardial knock). Associated with a loud S1, a Characteristics that may be used to differentiate a pericardial loud P2 with associated knock from other diastolic sounds are listed in Table 33. Pulsus pulmonary hypertension, and a low-pitched diastolic paradoxus is less frequent in constrictive pericarditis than in rumble at the apex cardiac tamponade. Peripheral edema, ascites, hepatomegaly, Pericardial Constrictive High frequency and pleural effusions are common. Muscle wasting may be knock pericarditis Heard throughout the evident in advanced cases. precordium An ECG is obtained as part of the initial evaluation and Earlierthan an 53 may reveal low voltage; however, no ECG findings are specific to constrictive pericarditis. Associated with deep x and y descents in the jugular Diagnosis of constrictive pericarditis is made with imaging venous pulse waveform studies and hemodynamic evaluation. Transthoracic echocar- Tumor plop Atrial Low frequency diography reveals normal right and left ventricular size and myxoma Heard best at the apex systolic function despite prominent symptoms and findings suggestive of heart failure. Dilatation ofthe inferior vena cava May be positional reflects elevated right-sided filling (right atrial) pressure. Dop- s3 Heart failure Low frequency pler echocardiography and tissue Doppler velocity are required Heard best at the apex and to differentiate constrictive pericarditis from restrictive cardio- the left lateral decubitus position myopathy (see Myocardial Disease). Myocardial relaxation is unimpaired or even enhanced in constrictive pericarditis, in Displaced point of maximal impulse which early diastolic filling is rapid and unimpeded, whereas relaxation is impaired in restrictive cardiomyopathy. Chest radiography or CT in constrictive pericarditis may Cardiac catheterization can be performed when con demonstrate partial or circumferential pericardial calcification strictive pericarditis is suspected but not confirmed by (Figure aS), and pericardial thickening (>3 mm) may be visible echocardiography. Invasive hemodynamic findings of con- on CT or CMR imaging. Importantly, constriction may exist in strictive pericarditis include a prominent y descent in the the absence of these findings. In one case series, hemody- right atrial waveform, which corresponds with the dip of namically proven constrictive pericarditis occurred with nor the right ventricular dip and plateau waveform (square mal pericardial thickness in 18% of cases. CMR imaging also root sign). The significant U descent and the right ventricu may demonstrate an inspiratory septal shift, a sign of ventricu- lar dip both represent unimpeded or rapid early diastolic lar interdependence. ventricular filling. As inflow volume reaches the fixed circumferential pericardial calcification (arorvs).

On physical examination, the central venous pressure is TABLE 33. Characteristics of the Selected Diastolic elevated in nearly all patients, with prominent x and y Heart Sounds descents. The height of the waveform does not fall or may Diastolic Condition Characteristics increase during inspiration (Kussmaul sign), reflecting the Heart Sound fixed diastolic volume of the right heart. Early diastolic filling Opening snap Mitral High frequency is unimpaired or even accentuated and is followed by sudden stenosis Heard best at the left lower cessation when total acceptable volume is met, resulting in a sternal border and the apex high-frequency early diastolic sound (the pericardial knock). Associated with a loud S1, a Characteristics that may be used to differentiate a pericardial loud P2 with associated knock from other diastolic sounds are listed in Table 33. Pulsus pulmonary hypertension, and a low-pitched diastolic paradoxus is less frequent in constrictive pericarditis than in rumble at the apex cardiac tamponade. Peripheral edema, ascites, hepatomegaly, Pericardial Constrictive High frequency and pleural effusions are common. Muscle wasting may be knock pericarditis Heard throughout the evident in advanced cases. precordium An ECG is obtained as part of the initial evaluation and Earlierthan an 53 may reveal low voltage; however, no ECG findings are specific to constrictive pericarditis. Associated with deep x and y descents in the jugular Diagnosis of constrictive pericarditis is made with imaging venous pulse waveform studies and hemodynamic evaluation. Transthoracic echocar- Tumor plop Atrial Low frequency diography reveals normal right and left ventricular size and myxoma Heard best at the apex systolic function despite prominent symptoms and findings suggestive of heart failure. Dilatation ofthe inferior vena cava May be positional reflects elevated right-sided filling (right atrial) pressure. Dop- s3 Heart failure Low frequency pler echocardiography and tissue Doppler velocity are required Heard best at the apex and to differentiate constrictive pericarditis from restrictive cardio- the left lateral decubitus position myopathy (see Myocardial Disease). Myocardial relaxation is unimpaired or even enhanced in constrictive pericarditis, in Displaced point of maximal impulse which early diastolic filling is rapid and unimpeded, whereas relaxation is impaired in restrictive cardiomyopathy. Chest radiography or CT in constrictive pericarditis may Cardiac catheterization can be performed when con demonstrate partial or circumferential pericardial calcification strictive pericarditis is suspected but not confirmed by (Figure aS), and pericardial thickening (>3 mm) may be visible echocardiography. Invasive hemodynamic findings of con- on CT or CMR imaging. Importantly, constriction may exist in strictive pericarditis include a prominent y descent in the the absence of these findings. In one case series, hemody- right atrial waveform, which corresponds with the dip of namically proven constrictive pericarditis occurred with nor the right ventricular dip and plateau waveform (square mal pericardial thickness in 18% of cases. CMR imaging also root sign). The significant U descent and the right ventricu may demonstrate an inspiratory septal shift, a sign of ventricu- lar dip both represent unimpeded or rapid early diastolic lar interdependence. ventricular filling. As inflow volume reaches the fixed circumferential pericardial calcification (arorvs). 89