PERICARDIAL DISEASES

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PERICARDIAL DISEASES:

PERICARDIAL DISEASES

WHAT IS PERICARDIUM ?:

WHAT IS PERICARDIUM ? Serous membrane covering of the heart and the root of great vessels Two layers – visceral & parietal layer with potential spacing between Parietal pericardium – pain sensitive

FUNCTIONS:

FUNCTIONS Lubricate surface of the heart Allows smooth and controlled movement of the heart in the thorax Barrier of infection

COMMMON PRESENTATIONS PERICARDIAL DISEASES :

COMMMON PRESENTATIONS PERICARDIAL DISEASES Pericarditis Pericardial Effusion Constrictive pericarditis

PERICARDITIS:

PERICARDITIS Inflammation of pericardium May develop pericardial effusion later Nature of fluid –serous, purulent or hemorrhagic Pericardium  thick and fibrinous exudate in between – bread and butter appearance

CLINICAL CLASSIFICATION:

CLINICAL CLASSIFICATION Acute pericarditis - < 6 weeks Fibrinous Serous Effusive Serosanguinous Subacute – 6 weeks to 6 months Effusive / Constrictive Chronic pericarditis Constrictive Effusive Adhesive

CAUSES:

CAUSES Myocardial Infarction Infections Viral (Coxsackie B, Echo) Mycobacterium Tuberculosis Staphylococci / H.Influenza Protozoa / Fungi Metabolic Uremia, Myxoedema

CAUSES:

CAUSES Connective Tissue disorders Rheumatoid Arthritis Rheumatic Fever Traumatic Post Irradiation Malignancies

CLINICAL FEATURES & DIAGNOSIS:

CLINICAL FEATURES & DIAGNOSIS Pain Pericardial friction rub ECG changes ECHO – Especially if pericardial effusion

PAIN:

PAIN Not invariable No pain in – uremic, tuberculous, neoplastic and post irradiation pericarditis Pain - retrosternally, may radiate to back / trapezius ridge Pleuritic in nature, changes with position, relief with sitting up and leaning forward

PERICARDIAL FRICTION RUB:

PERICARDIAL FRICTION RUB Most important physical sign of acute pericarditis Highly variable Classically triphasic  High pitched – Scratching – Grating Practically a to and fro leathery sound, may confuse with murmur Patient sitting leaning forward, in expiration- best heard

ECG:

ECG Requires serial ECGs Single ECG difficult ECG wise most important differential diagnosis is Acute Myocardial Infarction Acute phase ST elevation with upright T ST elevation in all leads except AVR and / V1 T inversion starts only after ST becoming iso-electric

Slide 17:

Chest X- Ray / ECHO may be useful when associated pericardial effusion present ECHO can detect even small amount of fluids – as low as 50 ml

PERICARDIAL EFFUSION:

PERICARDIAL EFFUSION Collection of fluid in the pericardial cavity Normally 15 to 20 ml May accommodate upto 50 ml normally ECHO can make out upto 50 ml of fluid Chest X-Ray become positive – atleast 250 ml Clinically can make out atleast 500 ml Rapid development of PE – cause tamponade

DIAGNOSIS - PE:

DIAGNOSIS - PE Pain – if associated with painful pericarditis Usual presentation as dyspnoea Peripheral pulse – pulsus paradoxis JVP – Elevation Apex – faint or not palpable Percussion – widening of cardiac borders Auscultation – Muffled heart sounds ECG – Low voltage complexes

PULSUS PARADOXUS:

PULSUS PARADOXUS Normal – during inspiration  systolic BP decreases (upto 10 mmHg is normal). Definition – Exaggeration of normal fall in systolic BP during inspiration. What is the paradox ? – during inspiration, peripheral pulses become feeble or absent, but mechanical activity of heart continues

X-RAY:

X-RAY Increased cardiac silhoutte – water bottle appearance Flask shaped enlargement with narrow pedicle Stenciled appearance of cardiac margins Cardio phrenic angle - acute

TAMPONADE:

TAMPONADE Accumulation of fluid in pericardial space beyond the distensibility of pericardium This leads to obstruction to the ventricular filling

TAMPONADE- PHYSIOLOGY:

TAMPONADE- PHYSIOLOGY Increase in intra cardiac pressure Decreased ventricular filling Decreased cardiac output

FACTORS INFLUENCING DEVELOPMENT OF TAMPONADE:

FACTORS INFLUENCING DEVELOPMENT OF TAMPONADE Rate of accumulation of fluid in effusion When acute, even 200 ml of fluid – produce tamponade. But Slow development of effusion, pericardium may even accommodate 2000 ml Thickness of ventricular myocardium

MANIFESTATIONS:

MANIFESTATIONS Dyspnoea, Orthopnoea Pulsus paradoxus Hypotension Raised JVP Kussmaul’s – Absent / very rare. Widening of cardiac dullness – percussion ECG – Electrical alternans involving P,QRS, T waves

CONSTRICTIVE PERICARDITIS:

CONSTRICTIVE PERICARDITIS Pericardium undergoes thickening, fibrosis and calcification (in response to chronic inflammation) Forms a tough cover – encasing heart – restrict diastolic filling LV function is preserved till date

CAUSES:

CAUSES Usually secondary to chronic inflammation Tuberculous pericarditis Hemopericardium Pyogenic, Uremic, Rheumatoid disease - rare May be a late complication of open heart surgery

MANIFESTATIONS:

MANIFESTATIONS Typically features of systemic venous congestion Increased JVP, Hepatomegaly, Ascites, Pedal Oedema Impaired filling of ventricles Pulsus Paradoxus Kussmaul’s sign Heart sounds muffled or distant ECG – low voltage, diffuse T wave changes

RADIOLOGICAL FEATURES:

RADIOLOGICAL FEATURES Chest X- Ray - Pericardial calcification may be seen. ECHO - Helpful, but may not be able to exclude pericardial thickening CT - Useful to establish or exclude pericardial thickening / calcification

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