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

1. PERICARDIAL DISEASES-2
Ajay Kumar Yadav
PGY3,Medicine
IOM-TUTH, Kathmandu

2. CONSTRICTIVE PERICARDITIS

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. 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. 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. 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.

8. 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.

10. 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

11. 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.

13. 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

14. 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).

15. 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.

17. 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.

20. Constrictive Vs Restrictive Cardiomyopathy

22. 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.

23. • 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.

24. EFFUSIVE-CONSTRICTIVE PERICARDITIS

25. • 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.

27. REFERENCE
• Braunwald’s Heart Disease 11th Edition
• Harrison 19th Edition
• UpToDate 2018
• Davidson’s 23rd Edition