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22 Cards in this Set
- Front
- Back
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Pericardial anatomy
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Fibrous parietal pericardium - outer layer which provides a protective sac around the heart to prevent sudden cardiac dilation and minimize bulk cardiac motion
Visceral pericardium - inner layer which is intimately related to the surface of the heart The two layers are separated by 10-50 ml of fluid. This fluid acts as a lubricant to minimize frictional forces between the heart and other structures. |
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Congenital pericardial abnormalities
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Absence of Pericardium: Partial or Total
- Usually diagnosed with CT or MRI - Associated with atypical chest pain or sudden death Pericardial cysts |
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Infectious pericarditis causes
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Viral (coxsackie A & B, echovirus, mumps, adenovirus, HIV)
Mycobacterium tuberculosis Bacterial (Pneumococcus, Streptococcus, Staphylococcus, Legionella) Fungal (histoplasmosis, coccidioidomycocis, candidiasis, blastomycosis) Viral pericarditis is the most common cause of pericarditis |
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Noninfectious pericarditis causes
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Idiopathic
Neoplasm -Metastatic (lung, breast, melanoma, lymphoma) -Primary (mesothelioma) Renal Failure/Uremia Irradiation Myocardial Infarction Hypothyroidism Aortic Dissection Chylopericardium (thoracic duct injury) Trauma -Post-pericardiotomy -Chest wall injury/trauma |
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Hypersensitivity pericarditis causes
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Collagen Vascular Disease (systemic lupus erythematosus, rheumatoid arthritis, scleroderma, acute rheumatic fever)
Drug Induced (procainamide, hydralazine, isoniazid) Post Myocardial Infarction or Cardiac Surgery - Dressler’s Syndrome(late presentation) |
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Acute pericarditis: clinical presentation
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Chest Pain:
usually sudden and severe in onset with viral pericarditis, usually 1-2 weeks after “viral illness” retrosternal or left precordial pain - may refer to back or trapezius pain may be preceded by low-grade fever may be pleuritic may be positional - worse with supine position; relieved with upright posture Physical Exam: resting tachycardia low-grade fever (if infectious etiology) pericardial friction rub on auscultation classically triphasic, but may be biphasic or monophasic |
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Acute pericarditis: diagnostic testing
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ECG
-diffuse ST-segment elevation in early stage -depression of the PR segment -T wave inversion in late stage -low voltage in QRS (if large pericardial effusion) -electrical alternans (if large pericardial effusion) -atrial fibrillation Laboratory Bloodwork - elevated erythrocyte sedimentation rate and white blood cell count Echocardiography - pericardial effusion may or may not be present |
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Pericarditis ECG
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In leads of "epicardial derivation" I, II, aVL, aVF, V3-V6
Stage I -ST elevation -T waves upright -Depression of PR Stage II early -ST isoelectric -T upright -PR depressed II late -ST isoelectric -T low to flat to inverted -PR seg isoelectric III -ST isoelectric -T inverted -PR isoelectric IV -ST isoelectric -T upright - PR isoelectric In leads of "endocardial derivation" aVR, V1 and sometimes V2 Stage I -ST depressed -T inverted -PR elevated or isoelectric Stage II early -ST isoelectric -T inverted -PR isoelectric or elevated Stage II late -ST isoelectric -T shallow to flat to upright -PR isoelectric or elevated Stage III -ST isoelectric -T upright -PR isoelectric Stage IV -ST isoelectric -T inverted -PR isoelectric |
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Acute pericarditis treatment
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If a significant pericardial effusion is not present, then treatment is targeted toward symptoms - usually with non-steroidal anti-inflammatory drugs.
If peri-infarct pericarditis, then may prefer high dose aspirin Steroids for resistant pericarditis Colchicine for resistant pericarditis |
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Pericardial effusion
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All forms of pericardial disease may lead to excess fluid accumulation in the pericardial space.
Any etiology for pericarditis is a potential cause for a pericardial effusion. Large effusions which accumulate slowly may be asymptomatic; rapidly accumulating smaller effusions may lead to cardiac tamponade. Serosanguinous effusions - neoplasm, Tb, uremia, idiopathic, non-infectious cause Hemopericardium - trauma, myocardial rupture, aortic dissection, coronary artery rupture Purulent effusion - secondary to direct invasion of the pericardial space by infectious organisms |
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Pericardial effusion: diagnosis
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Chest Radiograph - cardiomegaly or “water-bottle” shape
ECG - low voltage Echocardiography - imaging procedure of choice - size and location - characteristics of effusion - e.g. presence of fibrin, clot, tumor, calcium |
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Cardiac tamponade: pathophysiology
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Accumulation of fluid in the pericardial space leads to an increase in pericardial pressure .
Increased pericardial pressure may lead to cardiac compression resulting in impaired diastolic ventricular filling. This in turn depresses cardiac output. Cardiac tamponade is a clinical spectrum ranging from mild increases in pericardial pressure to profound hemodynamic collapse. |
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Cardiac tamponade: clinical presentation
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Presentation may mimic heart failure: Dyspnea on exertion and orthopnea
Tachycardia and tachypnea Jugular venous distention Hypotension and poor peripheral perfusion Shock and profound hemodynamic collapse Pulsus Paradoxus |
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Cardiac tamponade: diagnosis
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Clinical Presentation
Diagnostic Studies: - ECG - sinus tachycardia, electrical alternans - Echocardiography - signs of increased pericardial pressure - Cardiac Catheterization |
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Cardiac tamponade: treatment
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Supportive measures - intravenous fluids and pressors
Remove the fluid - pericardiocentesis - surgical pericardectomy |
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Constrictive pericarditis: pathophysiology
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Results from dense fibrosis and adhesion of the parietal and visceral layers
Creates a rigid “case” around the heart Early ventricular filling is unimpeded, but diastolic filling is subsequently abruptly reduced as a result of the inability of the ventricles to fill secondary to the restraints imposed by a rigid, thickened, and calcified pericardium. |
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Constrictive pericarditis: etiologies
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Anything that can cause pericarditis
Can develop acutely, sub-acutely(months), or sub-acutely(years) Common causes include neoplasm, tuberculosis, histoplasmosis, mediastinal radiation, purulent or recurrent pericarditis, rheumatoid arthritis, uremia, and cardiac surgery. Initial cause is often not identified. |
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Constrictive pericarditis: presentation
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Right heart failure
weakness, dyspnea, orthopnea, anorexia peripheral edema, hepatomegaly, splenomegaly, ascites, prominent y descent with jugular venous pressures “Kussmaul’s sign” - jugular venous filling with inspiration “pericardial knock”- characteristic abnormal sound in diastole |
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Constrictive pericarditis: diagnosis
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Can be very difficult to diagnose
Chest X-ray - pericardial calcification Echocardiography - signs of ventricular interdependence; respiratory variation in left and right ventricular filling Chest CT or MRI may identify pericardial thickening; CT may show pericardial calcification Cardiac catheterization |
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Constrictive pericarditis: treatment
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Poor Prognosis; Natural history is slow decline of cardiac output and progressive renal and hepatic failure.
Definitive treatment is surgical stripping of the pericardium |
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Cardiac trauma: penetrating injuries
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Bullet or stab wounds usually result in hemopericardium with tamponade or exsanguination.
May have associated cardiac damage such as traumatic valvular regurgitation, intracardiac shunts, and coronary artery injuries. Treatment: immediate thoracotomy for life-threatening hemorrhage or tamponade |
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Cardiac trauma: non-penetrating injuries
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Blunt trauma - most common cardiac manifestation is cardiac contusion
- new arrhythmias or ECG changes - LV wall motion abnormality on echo Other (less common) manifestations of blunt trauma include traumatic ventricular septal rupture, myocardial rupture and/or pseudoaneurysm formation, coronary artery trauma, valvular regurgitation, and pulmonary artery rupture. Traumatic Transection of the Descending Thoracic Aorta -Results from shear forces that occur during deceleration injury -More mobile arch continues to move anteriorly while the descending aorta remains fixed. -usually fatal if not rapidly repaired surgically |
