Pericarditis 1x PDF

PERICARDITIS Prof. Dr. A. Altug Cincin Department of Cardiology Pericardial Anatomy Two major components – serosa (viceral pericardium) mesothelial monolayer facilitate fluid and ion exchange – fibroa (parietal pericardium) fibrocollagenous tissue Pericardial Fluid in sac an...

PERICARDITIS Prof. Dr. A. Altug Cincin Department of Cardiology Pericardial Anatomy Two major components – serosa (viceral pericardium) mesothelial monolayer facilitate fluid and ion exchange – fibroa (parietal pericardium) fibrocollagenous tissue Pericardial Fluid in sac and recesses – 15 - 50 ml of clear plasma ultrafiltrate Ligamentous attachments, – to the sternum, vertebral column, diaphragm 2 Pericardium: Anatomy Pericardial Layers: Visceral layer Parietal layer  Function of the Pericardium SternoPericardial 1. Stabilization of the heart within the thoracic cavity by ligamnet and virtue of its ligamentous attachments -- limiting the heart’s motion. phernopericardial 2. Protection of the heart from mechanical trauma and infection from adjoining structures. 3. The pericardial fluid functions as a lubricant and decreases friction of cardiac surface during systole and diastole. In crease in intracardic indext is 4. Prevention of excessive dilation of heart especially during sudden rise in intra-cardiac volume (e.g. acute aortic or mitral assessed by x ray regurgitation). leading to In case of aortic and mitral regurgitation what is the structure that pervents excess ditlation of heart Diseases of the pericardium Diseases of the pericardium Pericarditis Pericardial effusions Cardiac tamponade Constrictive pericarditis Masses within the pericardium Congenital absence of Pericardium  Marafan syndrome is associated with Aortic regurgitation , metabolic Pericarditis syndrome with CAD and desslers sydrome with pericarditis, voice horansess with mitral stenosis Idiopathic Infectious (usually viral)- most common cause Inflammatory (usually autoimmune) Metabolic (uremia) Recent MI (Dressler’s syndrome) Metastatic cancer Clinical presentation of acute pericarditis Angina is a substernal pain not postional occurs Pleuritic and positional, retrosternal chest pain. on exerction Pericardial friction rub ECG cahnges; diffuse ST elevation or PR depression Pericardial effusion An other difference witn Mi we will see micardial injury markers like toroponin Chest Pain History pericarditis vs infarction Common characteristics – retrosternal or precordial with raditaion to the neck, back, left shoulder or arm Special characteristics (pericarditis) – more likely to be sharp and pleuritic – ↑ with coughing, inspiration, swallowing – worse by lying supine, relieved by sitting and leaning forward 11 ECG changes in Pericarditis 2/4 st e o st c Mo sitiv M sifi e sen sp Typical ECG changes in acute pericarditis: PR depression (↓) and concave ST-elevation (↑) 13  Which patients presenting with acute pericarditis should be hospitalized? Hospitalization is warranted for high-risk patients with an initial episode of acute pericarditis in order to determine a cause and to observe for the development of cardiac tamponade; close, early follow-up is critically important for the remainder of patients not hospitalized. Features indicative of high-risk pericarditis include fever greater than 38°C, subacute onset, an immunosuppressed state, trauma, oral anticoagulant therapy, myopericarditis, a moder- ate or large pericardial effusion, cardiac tamponade, and failure of initial outpatient medical therapy ECG differences in pericarditis... In a single ST segment deflection; rising leg of the T waves are convex shaped in ischemia but concave in pericarditis, In acute ischemia, the ECG changes are generally regional, but in acute pericarditis the changes are diffuse No reciprocal change in pericarditis unlike ischemia. Pericarditis should not lead to development of infarct patterns, namely Q waves or loss of R waves. T-wave inversion may happen in acute ischemia while the ST segments are still elevated; however, this pattern is uncommon in acute pericarditis as T-wave inversions occur after the ST segment has returned to baseline.  Friction rub 3/ 4 a superficial scratchy or squeaking sound best heard over the left sternal border; lying supine and at end expirium. High frequency...so heard with the diaphragm of the stethoscope Consists with three sounds: One systolic / two diastolic (early and late diastolic streching) Example: https://youtu.be/J1R8Oxgqhfk Pericardial effusion 4/ (new or worsening) 4 High risk criteria Major Minor – Fever < 38C – Myopericarditis – Subacute onset – Immunosupression – Large pericardial effusion – Trauma – Cardiac tamponade – Oral Anticougulant therapy – Lack of response to NSAID / ASA after 1 week Management Initial investigations; – To all suspected patients. – Physical examination, ECG, chest X-ray, echocardiogram, CRP, troponin Special investigations; – To patients with one of any high-risk criteria... – The epidemiologic backgorund should be considered (high vs. low tbc ?) Patients with high risk criteria should be investigated for nonviral causes of acute pericarditis. These patients warrants hospital admisson +/- inpatient treatment Treatment Treat underlying cause Anti-inflammatory drugs Colchicine Prednisone (recurrent, autoimmune causes) Treatment Treatment Restriction of exercise Corticosteroids Colchicine – in cases of contraindication/failure of aspirin/ NSAIDs and colchicine, – Only drug to prevent recurrency, – when there is a specific indication – >70kg 2x1 such as autoimmune disease – 3 months. – not recommended as first line therapy NSAID /ASA for acute pericarditis – CRP guided (1 – 2 weeks) – Protect GIS Recurrent pericarditis 15–30% of patients with idiopathic acute pericarditis who are not treated with colchicine will develop either incessant or recurrent pericarditis. %50 of patients with recurrent disease will experience one another recurrance Recurrance is established according to the same criteria as those used for acute pericarditis. CRP, CT and MR may provide confirmatory findings to support the diagnosis in atypical or doubtful cases A common cause of recurrence is inadequatetreatment of the first episode of pericarditis  Therapy for recurrent pericarditis Corticosteroids; – For patients with incomplete response to intial double therapy... Myopericarditis – Pericarditis with known or clinically suspected concomitant myocardial involvement should be referred to as ‘myopericarditis’ – Predominant myocarditis with pericardial involvement should be referred to as ‘perimyocarditis’, Chest pain associated with other signs of pericarditis +high troponin Treatment is similar with pericarditis. Constrictive pericarditis Scarring of both visceral and parietal layers constraining cardiac chambers Causes – Tuberculosis – Idiopathic or viral pericarditis – Mediastinal irradiation – Open heart surgery – CRF – Connective tissue disorders Physiology of Construction Pericardium acts as a calcified Shell Decreased compliance; – Rapid early diastolic filling, – Impaired late diastolic filling. Ventricular interdependence; – Pressure change in one chamber affects the other Enlarged great vessels – Intrathorasic pressure not transmitted to cardiac chambers Constructive pericarditis Restriction to cardiac filling Physiologic effect produced by constricting pericardium Gradual development of systemic and pulmonary venous hypertension – Atrial pressures 10-18 mmHg-systemic venous congestion – 18 to 30 mmHg-effort dyspnea, orthopnea Fall in stroke volume – Increased HR,systemic vascular resistance – Inability to augment cardiac output during exercise-fatigue – Cachexia Presentation of Constrictive Pericarditis Right sided congestion: edema, ascite, hepatic failure, fatigue, cachexia Left sided congestion: dyspnea, ortopnea, fatigue, cachexia Pericardial knock  Kussmaul’s Sign inspiration: ↓intrathoracic pressure, ↑ venous return to thorax ↓intrathoracic pressure not transmitted though to RV ⇒ no pulsus paradoxus! no inspiratory augmentation of RV filling (rigid pericardium) intrathoracic systemic veins become distended ⇒JVP rises with inspiration (normally falls) Rule-out; Restrictive cardiomyopathy* especially right sided. – In India endo myocardial fibrosis tops the list Primary Tricuspid valve disease – Tricuspid stenosis / Carcinoid syndrome etc Chronic cor-pulmonale with terminal RV failure Silent mitral stenosis with right heart failure Ebstein anomaly Severe forms of valvular pulmonary stenosis with RV dysfunction SVC obstruction Primary cirrhosis of liver Porto-pulmonary hypertension Treatment mainstay choice of treatment is surgery, medical therapy may have a role in at least three conditions. – 1- First, medical therapy of specific etiologies (i.e. tuberculous pericarditis) may be useful to prevent the progression to constriction. – 2- Reversibl forms.. Anti-inflammortory therapy for the transient constriction, generally as a temporary phenomenon during the resolution of pericarditis. (nearly %20) – 3- Advanced cases… medical therapy is supportive and aimed at controlling symptoms of congestion in advanced cases and when surgery is contraindicated or at high risk Medical therapy should never delay the surgery, if this option is feasible.