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Authors: Marc Sabatine
Tags: Medical, Internal Medicine
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steroids appear to ↑ rate of pericarditis recurrence ( Circ 2008;118:667).
• Avoid anticoagulants • Infectious effusion → pericardial drainage (preferably surgically) + systemic antibiotics • Acute idiopathic effusion self-limited in 70–90% of cases • Recurrent pericarditis ( Circ 2007;115:2739)
risk factors: subacute, lg effusion/tamponade, T >38°C, lack of NSAID response after 7 d treatment: add colchicine 0.5–1 mg bid × 6 mo ( Annals 2011;155:409)
• Recurrent effusion: consider pericardial window (percutaneous vs. surgical)
PERICARDIAL TAMPONADE
Etiology
• Any cause of pericarditis but esp. malignancy , uremia , idiopathic , proximal aortic dissection with rupture, myocardial rupture • Rapidly accumulating effusions most likely to cause tamponade as no time for pericardium to stretch (eg, to ↑ compliance) and accommodate ↑ intrapericardial fluid volume Pathophysiology ( NEJM 2003;349:684)
• ↑ intrapericardial pressure, compression of heart chambers, ↓ venous return → ↓ CO
• Diastolic pressures ↑ & equalize in all cardiac chambers → minimal flow of blood from RA to RV when TV opens → blunted y descent • ↑ ventricular interdependence → pulsus paradoxus (pathologic exaggeration of nl physio)
Inspiration → ↓ intrapericardial & RA pressures → ↑ venous return → ↑ RV size → septal shift to left. Also, ↑ pulmonary vascular compliance → ↓ pulm venous return. Result is ↓ LV filling → ↓ LV stroke volume & blood pressure.
Clinical manifestations
• Cardiogenic shock (hypotension, fatigue) without pulmonary edema • Dyspnea (seen in ~85%) may be due to ↑ respiratory drive to augment venous return Physical exam ( JAMA 2007;297:1810)
• Beck’s triad (present in minority of cases): distant heart sounds , ↑ JVP , hypotension • ↑ JVP (76%) w/ blunted y descent • Reflex tachycardia (77%), hypotension (26%; occasionally hypertensive), cool extremities • Pulsus paradoxus (Se 82%, Sp 70%) = ↓ SBP ≥10 mmHg during inspiration
LR 3.3 (5.9 if pulsus >12),LR 0.03
Ddx = PE, hypovolemia, severe COPD, constriction (~ 1 ⁄ 3 ), RV infarct
Can be absent if pre-existing ↑ LVEDP, arrhythmia, severe AI, ASD, regional tamponade
• Distant heart sounds (28%), ± pericardial friction rub (30%) • Tachypnea but clear lungs Diagnostic studies
• ECG: ↓ voltage (seen in 42%), electrical alternans (20%), ± signs of pericarditis • CXR: ↑ cardiac silhouette (89%) • Echocardiogram : effusion , IVC plethora, septal shift with inspiration
diastolic collapse of RA (Se 85%, Sp 80%) and/or RV (Se <80%, Sp 90%)
respirophasic Δ ’s in transvalvular velocities (↑ across TV & ↓ across MV w/ inspir.)
postsurgical tamponade may be localized and not easily visible
• Cardiac cath (right heart and pericardial): elevation (15–30 mmHg) and equalization of
intrapericardial and diastolic pressures (RA, RV, PCWP), blunted y descent in RA
↑ in stroke volume postpericardiocentesis = ultimate proof of tamponade
if RA pressure remains elevated after drainage, may have effusive-constrictive disease ( NEJM 2004;350:469) or myocardial dysfxn (eg, from concomitant myocarditis)
Treatment
• Volume (but be careful as overfilling can worsen tamponade) andinotropes (avoid bB) • Avoid vasoconstrictors as will ↓ stroke volume & potentially ↓ HR
• Pericardiocentesis (except if due to aortic or myocardial rupture, in which case
consider removing just enough fluid to reverse PEA en route to emergent surgery)
CONSTRICTIVE PERICARDITIS
Etiology ( Circ 2011;124:1270)
• Any cause of pericarditis (~1–2% incidence overall after acute pericarditis) • Highest risk w/ TB , bacterial , neoplastic , connective tissue, postcardiac surgery • Viral/idiopathic , as most common cause of pericarditis, also account for signif proportion Pathophysiology
• Adhesion of visceral and parietal pericardial layers → rigid pericardium that limits diastolic filling of
• Avoid anticoagulants • Infectious effusion → pericardial drainage (preferably surgically) + systemic antibiotics • Acute idiopathic effusion self-limited in 70–90% of cases • Recurrent pericarditis ( Circ 2007;115:2739)
risk factors: subacute, lg effusion/tamponade, T >38°C, lack of NSAID response after 7 d treatment: add colchicine 0.5–1 mg bid × 6 mo ( Annals 2011;155:409)
• Recurrent effusion: consider pericardial window (percutaneous vs. surgical)
PERICARDIAL TAMPONADE
Etiology
• Any cause of pericarditis but esp. malignancy , uremia , idiopathic , proximal aortic dissection with rupture, myocardial rupture • Rapidly accumulating effusions most likely to cause tamponade as no time for pericardium to stretch (eg, to ↑ compliance) and accommodate ↑ intrapericardial fluid volume Pathophysiology ( NEJM 2003;349:684)
• ↑ intrapericardial pressure, compression of heart chambers, ↓ venous return → ↓ CO
• Diastolic pressures ↑ & equalize in all cardiac chambers → minimal flow of blood from RA to RV when TV opens → blunted y descent • ↑ ventricular interdependence → pulsus paradoxus (pathologic exaggeration of nl physio)
Inspiration → ↓ intrapericardial & RA pressures → ↑ venous return → ↑ RV size → septal shift to left. Also, ↑ pulmonary vascular compliance → ↓ pulm venous return. Result is ↓ LV filling → ↓ LV stroke volume & blood pressure.
Clinical manifestations
• Cardiogenic shock (hypotension, fatigue) without pulmonary edema • Dyspnea (seen in ~85%) may be due to ↑ respiratory drive to augment venous return Physical exam ( JAMA 2007;297:1810)
• Beck’s triad (present in minority of cases): distant heart sounds , ↑ JVP , hypotension • ↑ JVP (76%) w/ blunted y descent • Reflex tachycardia (77%), hypotension (26%; occasionally hypertensive), cool extremities • Pulsus paradoxus (Se 82%, Sp 70%) = ↓ SBP ≥10 mmHg during inspiration
LR 3.3 (5.9 if pulsus >12),LR 0.03
Ddx = PE, hypovolemia, severe COPD, constriction (~ 1 ⁄ 3 ), RV infarct
Can be absent if pre-existing ↑ LVEDP, arrhythmia, severe AI, ASD, regional tamponade
• Distant heart sounds (28%), ± pericardial friction rub (30%) • Tachypnea but clear lungs Diagnostic studies
• ECG: ↓ voltage (seen in 42%), electrical alternans (20%), ± signs of pericarditis • CXR: ↑ cardiac silhouette (89%) • Echocardiogram : effusion , IVC plethora, septal shift with inspiration
diastolic collapse of RA (Se 85%, Sp 80%) and/or RV (Se <80%, Sp 90%)
respirophasic Δ ’s in transvalvular velocities (↑ across TV & ↓ across MV w/ inspir.)
postsurgical tamponade may be localized and not easily visible
• Cardiac cath (right heart and pericardial): elevation (15–30 mmHg) and equalization of
intrapericardial and diastolic pressures (RA, RV, PCWP), blunted y descent in RA
↑ in stroke volume postpericardiocentesis = ultimate proof of tamponade
if RA pressure remains elevated after drainage, may have effusive-constrictive disease ( NEJM 2004;350:469) or myocardial dysfxn (eg, from concomitant myocarditis)
Treatment
• Volume (but be careful as overfilling can worsen tamponade) andinotropes (avoid bB) • Avoid vasoconstrictors as will ↓ stroke volume & potentially ↓ HR
• Pericardiocentesis (except if due to aortic or myocardial rupture, in which case
consider removing just enough fluid to reverse PEA en route to emergent surgery)
CONSTRICTIVE PERICARDITIS
Etiology ( Circ 2011;124:1270)
• Any cause of pericarditis (~1–2% incidence overall after acute pericarditis) • Highest risk w/ TB , bacterial , neoplastic , connective tissue, postcardiac surgery • Viral/idiopathic , as most common cause of pericarditis, also account for signif proportion Pathophysiology
• Adhesion of visceral and parietal pericardial layers → rigid pericardium that limits diastolic filling of
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