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Pericardial diseases 2


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Continuation of pericardial diseases...worth to go through..wont disappoint

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Pericardial diseases 2

  1. 1. PERICARDIAL DISEASES-2 Ajay Kumar Yadav PGY3,Medicine IOM-TUTH, Kathmandu
  3. 3. ETIOLOGY • End stage of an inflammatory process involving the pericardium. • In the developed world the disorder is most commonly idiopathic or due to surgical complications or radiation injury. • TB : most common cause in developing countries. • The end result is fibrosis, often calcification, and adhesions of the parietal and visceral pericardium. • Scarring is usually more or less symmetric and impedes filling of all heart chambers.
  4. 4. Pathogenesis of TB CCP • Extension of infection from the lung or tracheobronchial tree, adjacent lymph nodes, spine, sternum, or via miliary spread. • Mostly reactivation disease, and the primary focus of infection may be inapparent. • Four pathological stages of tuberculous pericarditis have been described Fibrinous exudation with PMN leukocytosis, abundant mycobacteria, and early granuloma formation with loose organization of macrophages and T cells Serosanguineous effusion with lymphocytic exudate and high protein concentration; tubercle bacilli present in low concentrations Absorption of effusion with granulomatous caseation and pericardial thickening with subsequent fibrosis Constrictive scarring; fibrosing visceral and parietal pericardium contracts on the cardiac chambers and may become calcified, leading to constrictive pericarditis, which impedes diastolic filling
  5. 5. PATHOPHYSIOLOGY • The consequence of pericardial scarring is markedly restricted filling of the heart  results in elevated and equal filling pressures in all chambers and systemic and pulmonary veins. • In early diastole the ventricles fill rapidly because of markedly elevated atrial pressures and accentuated early diastolic ventricular suction related to small end-systolic volumes. • During early to mid-diastole, ventricular filling abruptly ceases when the cardiac volume reaches the limit set by the pericardium. • Thus, almost all filling occurs early in diastole. • Systemic venous congestion results in hepatic congestion, peripheral edema, ascites, anasarca, and cardiac cirrhosis. • Reduced cardiac output also results from impaired filling and causes fatigue, muscle wasting, and weight loss.
  6. 6. CLINICAL MANIFESTATIONS • S/S of RHF  Pedal edema  Congestive tender hepatomegaly  Ascites Precox  Anasarca  Jaundice (cardiac cirrhosis) • S/S of LHF  Dyspnea  Cough  PND and/or orthopnea • Atrial fibrillation and TR : common • Recurrent pleural effusions and syncope.
  7. 7. PHYSICAL EXAMINATION • Markedly elevated JVP • Apical impulse is reduced and may retract in systole (Broadbent’s sign ) • Prominent, rapidly collapsing y descent combined with normal x descent  venous pressure contour. M- or W-shaped • In patients with AF, the x descent is lost. • Kussmaul sign : usually present : inspiratory increase in JVP or the pressure may simply fail to decrease on inspiration. • Reflects loss of the normal increase in right heart venous return on inspiration.
  8. 8. Cont.. • The most notable cardiac physical finding is the pericardial knock • Early diastolic sound best heard at the left sternal border and/or the cardiac apex. • Occurs slightly earlier and has a higher frequency content than a third heart sound. • Corresponds to early, abrupt cessation of ventricular filling. • P/A examination : hepatomegaly, often with palpable venous pulsations, with ascites(precox). • Other signs of hepatic congestion/cirrhosis • Lower extremity edema is the rule. • Muscle wasting, cachexia
  9. 9. Laboratory Testing • No specific ECG findings. • Nonspecific T-wave abnormalities, reduced voltage, and LA enlargement may be present. • AF is very common. • CXR • Cardiac silhouette can be enlarged due to a coexisting pericardial effusion. • Pericardial calcification is seen in a minority of patients and suggests TB. • Pleural effusion common.
  10. 10. ECHOCARDIOGRAPHY • M-mode and two-dimensional transthoracic and Doppler echocardiography are primary imaging modalities in the evaluation of constrictive pericarditis . • Major findings include • Pericardial thickening and calcification (best appreciated with TEE), • Abrupt displacement of the IVS during early diastole (septal bounce), and • Signs of systemic venous congestion (dilation of hepatic veins, inferior vena caval distention with blunted respiratory variation). • LVEF is usually normal. • Mild to moderate (but not severe) biatrial enlargement is common
  11. 11. Cardiac Catheterization and angiography • The RA and RV diastolic pressure, pulmonary capillary wedge pressure, and pre–a wave LV diastolic pressure are elevated and equal, or nearly so, at around 20 mm Hg. • Differences of more than 3 to 5 mm Hg between the left and right heart filling pressures are rare. • The RA pressure tracing shows a preserved x descent, a prominent y descent, and roughly equal a-wave and v-wave heights, with a resultant M or W configuration. • RV and LV pressures reveal an early, marked diastolic dip followed by a plateau (dip-and plateau, or square root sign).
  12. 12. Cont.. • Respiratory variation in the LV and RV systolic and diastolic pressures is increased. • Quantified using the systolic area index (ratio of RV to LV systolic pressures × time area in inspiration versus expiration). • A ratio higher than 1.1 strongly suggests constriction • Pulmonary artery and RV systolic pressures are often modestly elevated to 35 to 45 mm Hg. • Hypovolemia (e.g., due to diuretic therapy) can mask hemodynamic findings Infusion of 1 L of normal saline over 6 to 8 minutes may reveal typical features. • The SV is reduced, but cardiac output can be preserved because of tachycardia.
  13. 13. CT and MRI • CT • Helpful in detecting even minute amounts of pericardial calcification and is the most accurate method for measuring thickness (normal < 2 mm) • Its major disadvantage is the frequent need for iodinated contrast medium to best display pericardial pathology. • MRI • Detailed examination of the pericardium without the need for contrast or ionizing radiation. • Less sensitive for detecting calcification than CT and less accurate for measuring thickness. • The “normal” pericardium visualized by MRI is up to 3 to 4 mm in thickness.
  14. 14. Constrictive Vs Restrictive Cardiomyopathy
  15. 15. MANAGEMENT • Surgical pericardiectomy is the definitive treatment. • Pericardiectomy can be performed through a median sternotomy or a left fifth interspace thoracotomy and involves radical excision of as much parietal pericardium as possible • Relatively high perioperative mortality rate, ranging from 2% to nearly 20% • Risk factors for poor outcomes • Radiation-induced disease; • Comorbidities, esp. COPD and renal insufficiency; CAD and prior cardiac surgery; • Reduced LV EF; • Cardiopulmonary bypass; and • NYHA stage IV symptoms.
  16. 16. • Diuretics and salt restriction are used to relieve the volume overload, but patients ultimately become refractory. • Because sinus tachycardia is compensatory, beta-adrenergic blockers and CCBs that slow the HR should be avoided. • In patients with AF and FVR : digoxin is recommended for rate control. • WAFFLE PROCEDURE • Multiple transverse and longitudinal incisions are made in the epicardial layer. • An alternative t/t in pts with extensive epicardial involvement.
  18. 18. • ECP combines elements of effusion/ tamponade and constriction. • A proposed definition of underlying constriction is the failure of RA pressure to decline by at least 50% to a level below 10 mm Hg when pericardial pressure is reduced to almost 0 mm Hg by pericardiocentesis and/or all detectable fluid is removed. • Incidence : 1-15% , high in TB. • The most common causes of ECP are cancer, irradiation, TB, complications following pericardiotomy, and CTD. • Management is tailored to the specific cause, if known. • Pericardiectomy is ultimately required in many pts.
  19. 19. REFERENCE • Braunwald’s Heart Disease 11th Edition • Harrison 19th Edition • UpToDate 2018 • Davidson’s 23rd Edition