Pericardium diseases and cardiac neoplasms Flashcards
Chronic pericardial effusion
<500 mL and globular enlargement of heart shadow on CXR
Pericardial fluid under pressure leading to impaired diastolic filling of ventricles and elevated venous pressures
Cardiac tamponade
Scarred, rigid pericardium leading to impaired diastolic filling of ventricles, SV, and decreased CO
Constrictive pericarditis
Pressure tracing change in cardiac tamponade
Flattening of y descent
Decrease of SBP by >10 mmHg during normal inspiration, seen in cardiac tamponade
Pulsus paradoxus
How to check for pulsus paradoxus
Find highest pressure at which first Korotkoff sound is heard. Then further deflate until sound is Korotkoff is heard in inspiration and expiration. Should be <10 mmHg difference.
Clinical features of acute pericarditis
Fever
Severe CP, retrosternal
Sharp, pleuritic, and positional CP
Pericardial friction rub
Movement of inflamed pericardial layers against one another heard on auscultation when pt leans forward and exhales.
Pericardial friction rub
EKG findings in pericarditis
Diffuse ST segment elevation in majority of leads
Possible cause of serous pericarditis
Rheumatic fever
SLE
Scleroderma
Tumors
Infection of tissues contiguous to pericardium
Uremia
Exudate in serous pericarditis
Thin fluid secreted by mesothelial cells. Contains lymphocytes.
Possible causes of fibrinous and serofibrinous pericarditis
Acute MI
Dressler syndrome
Uremia
Rheumatic fever
SLE
RA
Trauma
Most frequent types of pericarditis
Fibrinous and serofibrinous
Exudate in fibrinous pericarditis
Contains plasma proteins, including fibrinogen.
Grossly rough, granular, dry, and shaggy appearance of pericardium
Fibrinous pericarditis
Exudate in purulent or suppurative pericarditis
Thin and cloudy to frank pus
400-500 mL
Complication of purulent or suppurative pericarditis
Constrictive pericarditis
Exudate in hemorrhagic pericarditis
Blood mixed with a fibrinous or suppurative effusion
Most common cause of hemorrhagic pericarditis
Spread of malignant neoplasm to pericardial space
TB
Causes of chronic constrictive pericarditis
TB
Remote history of idiopathic or viral acute pericarditis
Prior radiation to L chest
Pathogenesis of chronic constrictive pericarditis
Fluid undergoes organization and then fusion of pericardial layers. Followed by fibrous scar formation, which may calcify.
Clinical features of chronic constrictive pericarditis
Reduced CO –> fatigue, hypotension, and reflex tachycardia
Elevated systemic venous pressures
Pulsus paradoxus, not prominent
Kussmaul sign
Paradoxical increase in JVP during inspiration
Kussmaul sign
Clinical findings of elevated systemic venous pressures
Jugular venous distension
Hepatomegaly with ascites
Peripheral edema
Most common primary tumor of the adult heart
Myxomas
Benign neoplasm of the heart that arises from primitive multipotent mesenchymal cells.
Myxomas
Conditions associated with myxomas
McCune-Albright syndrome
Carney complex
Syndrome characterized by activating mutations in GNAS1 gene that encode a subunit of G protein
McCune-Albright syndrome
Syndrome characterized by mutations in PRKAR1A that encodes a regulatory subunit of cAMP dependent protein kinase
Carney complex
Cause of fever and weight loss in myxoma
Production of IL-6
Clinical features of myxoma
Early diastolic tumor plop sound
Syncope
Most common locations of myxoma
90% in atria, L>R
Position where myxoma may obstruct mitral flow more easily
Upright positon
Platypnea
Dyspnea that improves with laying flat
Single, sessile or pedunculated lesion in the LA. May be a globular hard mass mottled with hemorrhage OR a soft, translucent, papillary or villous lesion with gelatinous appearance.
Myxoma
Microscopy of LA mass shows stellate or globular cells embedded within an abundant acid mucopolysaccharide ground substance. With peculiar vessel-like or gland-like structures
Myxoma
Most frequent primary tumor of pediatric heart
Rhabdomyoma
Obstruction of a valvular orifice or cardiac chamber discovered in first year of life. Associated with tuberous sclerosis in 50% of cases.
Rhabdomyoma
TSC1 or TSC2 expression absent leading to myocyte overgrowth.
Rhabdomyoma associated with tuberous sclerosis
Frequent major features of tuberous sclerosis
Facial angiofibromas
Hypomelanotic macules
Cortical tubers
Subependymal nodules
Common major features of tuberous sclerosis
Retinal hamartomas
LAM
Renal AML
Cardiac rhabdomyomas
Uncommon major features of tuberous sclerosis
Shagreen patches
Ungual fibromas
Subependymal giant cell tumors
Frequent minor features of tuberous sclerosis
Multiple pits in dental enamel
Hamartomatous rectal polyps
Common minor features of tuberous sclerosis
Bone cysts
Cerebral white matter radial migration lines
Multiple renal cysts
Gingival fibromas
Uncommon minor features of tuberous sclerosis
Confetti skin lesions
Retinal achromatic patches
Cause of carcinoid heart disease
Bioactive compounds (like serotonin) released by carcinoid tumors
Reason that carcinoid heart disease typically only occurs when there is a massive hepatic metastatic burden
Liver normally metabolizes circulating mediators before they reach the heart
Pearl white fibrosis of the tricuspid valve with tricuspid regurgitation. Increased plasma levels of serotonin.
Carcinoid heart disease
Reason that L heart is protected in carcinoid heart disease
Mediators are degraded in pulmonary vascular bed
Serotonin metabolite excreted in urine in carcinoid syndrome
5-HIAA
Single most important long-term limitation of cardiac transplant
Allograft arteriopathy
Late, progressive, diffusely stenosing intimal proliferation in the coronary arteries leading to ischemic injury. Caused by production of growth factors that promote intimal smooth muscle cell recruitment and proliferation with ECM synthesis
Allograft arteriopathy in heart transplant
Complications of allograft arteriopathy in heart transplant
Silent MI
Progressive CHF
Sudden cardiac death
Timeframe for development of allograft arteriopathy in heart transplant pts
Within 10 yrs
