Several Slides courtesy of Alena Goldman, M.D. Pericardial Diseases Several Slides courtesy of Alena Goldman, M.D. 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Pericardium Fibroelastic sack made up of visceral and parietal layers separated by a potential space, pericardial cavity Forms a sac enclosing the origin of the aorta, pulmonary artery, Pulmonary veins, venae cavae 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Categories 3 major categories of pericardial diseases (co-existing, overlaping with one another): Pericarditis (inflammation of the pericardium) Pericardial effusion (fluid around the heart causing clinical presentation from asymptomatic to causing tamponade) Constrictive pericarditis (inelastic sac that impairs filling) Pericardial effusion and cardiac tamponade really a continuous spectrum of diseases. 2008 Zoll Firm Lecture Series
Etiology of pericardial Diseases Idiopathic pericarditis Infectious (viral, bacterial, Mycoplasma, fungal, parasitic) Vasculitis/connective tissue disease (lupus, RA, scleroderma, MCTD, Wegener’s, PAN, sarcoid, IBD, Whipple’s, GCA, Behcet’s) Hypersensitivity/immunopathies Diseases of contiguous structures (post-infarction/early, Dressler’s, myocarditis, dissecting aortic aneurism) Disorders of metabolism (hypothyroidism, uremia, ovarian hyperstimulation syndrome) Trauma (blunt, penetrating, iatrogenic) Neoplasms (mets, primary, paraneoplastic) Other (congenital) 2008 Zoll Firm Lecture Series
Acute Pericarditis: Clinical Presentation Symptoms Left precordial chest pain (pleuritic, worsens with recumbency; relieved with leaning forward, sudden onset) Fever Malaise, myalgias Symptoms of systemic illness, depending on the etiology Signs Pericardial friction rub (easier to hear in an absence of an effusion): Three phases: correspond to movement of the heart during atrial systole ventricular systole, and in the rapid filling phase of early ventricular diastole serum biomarkers for myocardial injury: related to the extent of myocardial inflammation Elevated WBC, CRP 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series ECG Changes Low Voltage Electrical Alternans (“Cardiac Nystagmus” by Littman) ST Segment Deviation PR Segment Changes TWI 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series EKG changes Stage I- diffuse PR depression, ST elevation except in avR and v1 (the typical pericarditis EKG). Stage II- (several days later) PR and ST segments normalized, T wave becomes flat. Stage III- diffuse T wave inversion Stage IV- resolution (several days to weeks) 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Typical ECG (stage I) 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Echocardiography Acute pericarditis is a clinical diagnosis. Echocardiogram is often normal in patients with acute syndrome unless it is associated with a pericardial effusion Finding of a pericardial effusion in a patient with known or suspected pericarditis supports the diagnosis, the absence of a pericardial effusion or other echocardiographic abnormalities does not exclude it Do not need to order it unless you suspect substantial pericardial effusion. 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series 2D Echo 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Identifying the Cause In Western countries, most cases of acute pericarditis in immunocompetent patients that are not associated with apparent medical or surgical conditions are due to viral infection (entero-, echo-, adenoviruses; CMV, EBV, HSV, influenza, parvo, HCV, HIV) or are idiopathic A full diagnostic evaluation is not appropriate in all patients 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series 2008 Zoll Firm Lecture Series Maisch, B., Heart 2003; 89
Zoll Firm Lecture Series Management For symptom relieve: NSAIDs- indomethacin 25-50mg PO TID or ibuprofen 600-800mg PO TID for 3 weeks Cholchicine- 1mg/d for 3 weeks Steroids- less preferred, patient’s symptoms often rebound when steroids are withdrawn. If needed- prednisone 40-60mg PO qd x 3wks 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Complications Recurrent in 20-30% of the cases. Infrequently, can progress to tamponade or constriction. None of the medical therapy has been vigorously proven to prevent complications. 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Pericardial effusion Can be asymptomatic or present as life-threatening cardiogenic shock (tamponade). Can also present in between the above two polar opposites. Symptoms occur when increase in pericardial fluid raises the intrapericardial pressure and impairs diastolic filling. The presenting syndrome depends on the: Volume (bigger worse) rate of accumulation (faster worse) Characteristic (thicker worse) 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Cardiac Tamponade Tamponade is at one extreme of the of the syndrome and is characterized by: Progressive increase in intrapericardial pressure first becoming equal to the RV then later the LV filling pressures (equalization of diastolic pressure) Continual elevation of intracardiac filling pressure. Impairment of diastolic filling Lack of filling leads to fall in cardiac output. At first, the body compensates through tachycardia and vasoconstriction. As the syndrome progresses, this mechanism becomes inadeqaute and shock ensues. Needs to be treated by urgent pericardiocentisis. 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Relationship Between Intracardiac Filling Pressures and Intrapericardial Pressure and Cardiac Output in Cardiac Tamponade Slide 2 Roy, C. L. et al. JAMA 2007;297:1810-1818. 2008 Zoll Firm Lecture Series Copyright restrictions may apply.
Clinical presentation Symptoms Mostly relates to low cardiac output and high filling pressure. Mental status changes Dypsnea Signs: Low BP Tachycardia Tachypnea Diminished heart sounds Low urine output Pulsis paradoxus- inspiratory decline in SBP >10mmHg. 2008 Zoll Firm Lecture Series
Measurement and Mechanism of Pulsus Paradoxus Roy, C. L. et al. JAMA 2007;297:1810-1818. 2008 Zoll Firm Lecture Series Copyright restrictions may apply.
Echocardiography in cardiac tamponade Visualizes the effusion Impairment of diastolic filling causes the cardiac chambers to be “squashed” 1st RA collapse (lowest pressure chamber, more sensitive, less specific) 2nd RV collapse (fairly specific) False negative in the presence of substantial pulmonary hypertension. variation in mitral and tricuspid inflow. Ultimately, cardiac tamponade is a clinical diagnosis though echocardiogram is very useful in this setting 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Echocardiogram of a 62-Year-Old Woman With Advanced Lung Cancer and Malignant Pericardial Effusion Causing Cardiac Tamponade Roy, C. L. et al. JAMA 2007;297:1810-1818. 2008 Zoll Firm Lecture Series Copyright restrictions may apply.
Zoll Firm Lecture Series Diastolic RA collapse 2008 Zoll Firm Lecture Series
Constrictive Pericarditis Typically, long delay between onset of constriction and pericardial inflammation Common etiologies includes radiation, TB…etc. Although many pericardial diseases can lead to constriction. Presents with R>L sided failure symptoms Insidious symptoms at first, followed by dypsnea with exertion, orthopnea, edema…etc. Diagnosed by a combination of Echocardiography (pericardium, filling patterns, interventricular dependence…etc) chest CT/MRI (better at defining pericardium) RHC (gold standard for hemodynamic assessment) Pericardiectomy is the only therapy for a permanent constriction 2008 Zoll Firm Lecture Series
Constrictive Pericarditis - Pathophysiology Fibrosed or calcified pericardium restricts diastolic filling of all 4 chambers constriction leads to elevated and equilibrium of the diastolic pressures In early diastole filling is unimpaired => abnormally rapid filling filling is abruptly halted when cardiac volume meets the limits determined by the stiff pericardium Virtually all filling occurs during early diastole 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series CXR dense circumferential calcification of pericardium 2008 Zoll Firm Lecture Series
Zoll Firm Lecture Series Chest CT demonstrating extent and severity of pericardial calcification Circulation. 2005;112:e137-e139 2008 Zoll Firm Lecture Series