DISEASES OF THE PERICARDIUM 1-ACUTE PERICARDITIS 2-PERICADIAL EFFUSION (AND CARDIAC TAMPONADE) 3-CONSTRICTIVE PERICARDITIS

THE PERICARDIUM Structure and function Functions Protective sac around heart, two distinct layers outer fibrous pareital & inner visceral Contains == 50 ml of fluid similar to lymph- lubricates surface of heart. Functions 1- limits distension of heart 2- haemodynamic interdependence of ventricles 3-barrier to infection.

1-ACUTE PERICARDITIS Inflammation of visceral and parietal layers AETIOLOGY infection, immunological reaction, trauma neoplasm unexplained. Pericarditis and myocarditis often coexist, 1-Common causes 1-Viral (e.g. Coxsackie B, but often not identified) 2-Acute myocardial infarction 2- Less common 3- Rare (in UK) Uraemia Bacterial infection Malignant disease Rheumatic fever Trauma (e.g. blunt chest injury) Tuberculosis Connective tissue disease (e.g. SLE)

Pathological types 1-fibrinous 2-serous 3-haemorrhagic 4-purulent. 1- fibrinous exudate  varying degrees of adhesion formation, 2- serous pericarditis  large effusion - turbid, straw-coloured fluid +high protein content. 3- haemorrhagic effusion = malignant disease, part. Ca. breast, ca. bronchus and lymphoma. 4-Purulent = rare complication of septicaemia direct spread -- intrathoracic infection / penetrating injury

Clinical features TRIAD =Chest pain +fever+ Pericardial rub Retrosternal, Radiates to shoulders and neck Aggravated by deep breathing, movement change of position exercise swallowing. 2- fever- low-grade 3- pericardial friction rub- diagnostic high-pitched superficial scratching or crunching noise produced by movement of inflamed pericardium, usually heard in systole but may also be audible in diastole frequently has a 'to-and-fro' quality.

Investigations ECG Chest x-ray and echocardiography  ST elevation -upward concavity( over affected area)- widespread. PR interval depression – very sensitive indicator of acute pericarditis. T-wave inversion,(Later) esp. if there is a degree of myocarditis Chest x-ray and echocardiography  normal in most cases (unless complicated by effusion)

Treatment Pain = aspirin (600 mg 4-hourly) Outcome indometacin (25 mg 8-hr.). more potent anti-inflammatory Corticosteroids may suppress symptoms – no evidence that they accelerate cure. Outcome 1- viral pericarditis= recovery usually occurs within few days or weeks, ----recurrences (chronic relapsing pericarditis). 2-Purulent pericarditis antimicrobial therapy, paracentesis if necessary, surgical drainage.

2-PERICARDIAL EFFUSION Abnormal accumulation of fluid within pericardial space TYPES Small= hemodynamically insignificant effusion  generally asymptomatic Large  chest pressure or symptoms related to compression of adjacent structures Hemodynamic consequences of PE  rate of fluid accumulation rather than size slowlymay accommodate up to 2 liters without P.pressure rapid 100-200 ml. may result in cardiac tamponade

Clinical Features difficult to detect clinically; 1- sensation of retrosternal oppression. 2-apical impulse ----difficult to palpate 3-heart sounds --- quieter, 4- pericardial friction- ( not always abolished).

INVESTIGATIONS ECG CXR Echocardiography CT & MRI- detect the cause

ECG: QRS voltages - reduced in presence of large effusion ECG: QRS voltages - reduced in presence of large effusion. QRS complexes - alternate in amplitude { to-and-fro motion of heart within fluid-filled pericardial sac }(electrical alternans).

Radiologically: Serial chest X-rays = rapid increase in size of cardiac shadow over days or even hours, large effusion = heart often has globular or pear-shaped appearance

Echocardiography definitive investigation for detection ,size ,location and H-D significance

CT and MRI detect the cause

Cardiac tamponade Aetiology collection of fluid or blood in the pericardial sac, compressing the heart effusion may be small and is very occasionally less than 100 mL. =acute heart failure due to compression of heart by a large or rapidly developing effusion Typical physical findings =markedly raised JVP,hypotension,pulsus paradoxus and oliguria. Atypical presentations =effusion is loculated (result of previous pericarditis or cardiac surgery.) Sudden deterioration may be due to bleeding into the pericardial space. Aetiology complication of pericarditis malignant disease. trauma rupture of t free wall of the myocardium following MI.

Clinical features of pericardial tamponade Dyspnoea Collapse Tachycardia Hypotension Gross elevation of the JVP Soft heart sounds with an early third heart sound Pulsus paradoxus (a large fall in BP during inspiration, when the pulse may be impalpable) Kussmaul’s sign (paradoxical rise in JVP during inspiration

- ECG features of underlying disease, e.g.pericarditis or acute MI. large pericardial effusion=ECG complexes are small electrical alternans: changing axis with alternate beats caused by t heart swinging from side to side in the pericardial fluid. Chest X-ray enlarged globular heart but can look normal. Echocardiography – confirming t diagnosis identify the optimum site for aspiration of the fluid. Prompt recognition of tamponade is important because the patient usually responds dramatically to percutaneous pericardiocentesis or surgical drainage

Cardiac Tamponade Compression heart by a large or rapidly developing effusion acute heart failure

Pericardial aspiration Indicated for diagnostic purposes or treatment of cardiac tamponade. Accomplished by introducing needle just medial to cardiac apex or by inserting a needle below the xiphoid process + simultaneous echo. Amount few millilitres of fluid -sufficient for diagnostic purposes; therapeutic drainage - a plastic cannula inserted over a needle or guidewire. Complications of pericardiocentesis= arrhythmias damage to coronary artery bleeding with exacerbation of tamponade - injury to the right ventricle. When tamponade due to cardiac rupture or aortic dissection P. aspiration may precipitate further bleeding == emergency surgery

TUBERCULOUS PERICARDITIS 1-Complicatiion pulmonary tuberculosis /first manifestation 2-In Africa, a tuberculous PE is a common feature of AIDS. Clinical features- 1-chronic malaise, 2-weight loss 3-low-grade fever. OUTCOME An effusion usually develops  tamponade. pericardium may become thick and unyielding pericardial constriction ( An associated pleural effusion is often present). Diagnosis – aspiration of the fluid and direct examination or culture for tubercle bacilli. Treatment- Antituberculous chemotherapy + 3-M course of prednisolone (initial dose 60 mg a day, tapering down rapidly =improve outcome.

3-CHRONIC CONSTRICTIVE PERICARDITIS progressive thickening, fibrosis and calcification =pericardium. Heart = encased in a solid shell and cannot fill properly; calcification may extend into the myocardium- impaired myocardial contraction Atiology often follows an attack of tuberculous pericarditis Complication of haemopericardium viral pericarditis rheumatoid arthritis purulent pericarditis.

- Clinical features symptoms and signs of systemic venous congestion atrial fibrillation = common dramatic ascites and hepatomegaly. Breathlessness is not prominent symptom ( lungs seldom congested.) suspected - unexplained right heart failure and a small heart. Fatigue Rapid, low-volume pulse Elevated JVP with a rapid y descent Kussmaul's sign (a paradoxical rise in the JVP during inspiration) Loud early third heart sound or 'pericardial knock' Hepatomegaly Ascites Peripheral oedema Pulsus paradoxus ( excessive fall in BP during inspiration in some cases

chest X-ray=show pericardial calcification), Investigations chest X-ray=show pericardial calcification), echocardiography = establish the diagnosis. CT and MRI = useful techniques for imaging the pericardium. Differential diagnosis often difficult to distinguish from restrictive cardiomyopathy final diagnosis may depend on complex echo-Doppler studies and cardiac catheterisation.

Management Surgical resection of the diseased pericardium = dramatic improvement carries a high morbidity  disappointing results in up to 50% of patients