PERICARDIAL DISEASES. GENERAL CONSIDERATIONS. The pericardium consists of two layers: the inner visceral layer, which is attached to the epicardium , and an outer parietal layer. About 50 mL of serous fluid is normally present and provides lubrication between the two layers.
Pericarditis and cardiac tamponade involve the potential space surrounding the heart or pericardium.
Pericarditis is one cause of fluid accumulation in this potential space and cardiac tamponade is the hemodynamic result of fluid accumulation.
I- Diffuse ST elevation and PR segment depression (seen in more than 80%)
II- Normalization of the ST and PR
III- Widespread T- wave inversions
IV- Normalization of the T waves
This 12-lead electrocardiogram is representative of pericarditis.
Stage 1 electrocardiograph changes in a patient with acute pericarditis.
Stage 2 ECG changes in patient with acute pericarditis obtained 3 days into clinical course.
Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardiocentesis (B).
This ultrasonogram demonstrates a normal subcostal 4-chamber view of the heart. The pericardium is brightly reflective (echogenic or white in appearance). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.
This is a modified subcostalultrasonographic view of the heart in which a thick anechoic (dark or black) stripe is seen surrounding the heart (H). The stripe represents a large amount of fluid (F) in the pericardium, indicating tamponade.
Electrocardiogram from a patient with massive malignant pericardial effusion showing electrical alternans. Note that all are sinus beats with the same PR interval, but that the QRS axis alternates.
This anteroposterior-view chest radiograph shows a massive bottle-shaped heart and conspicuous absence of pulmonary vascular congestion.
Several indicators of poor prognosis:
MRI fast spin echo image with blood suppression in a ventricular short-axis plane showing circumferential thickening of the pericardium (black rim between the epicardial and pericardial fat) (arrow).
(A) Apical four-chamber view showing pericardial effusion. (B) Modified apical view showing a spider-web appearance formed by the fibrin strands.
Systemic signs of venous congestion:
-Hepatomegaly and raised JVP
-Anorexia and postprandial fullness.
-markedly raised JVP with pominent “x” and “y” descent.
-Friedreich’s sign: raised JVP with sharp diastolic collapse.
-pericardial knock: early diastolic sound.
but usually are less frequent.
A 12-lead ECG from a young woman showing the most common electrocardiographic abnormality found in arrhythmogenic right ventricular cardiomyopathy, T-wave inversion in the precordial leads V1–V4.
Echocardiographic appearances of a young patient with familial dilated cardiomyopathy. Panel A: parasternal long-axis view showing significant left atrial (LA)
and biventricular dilatation with a thin intraventricular septum (IVS). Panel B: apical four-chamber view demonstrating dilatation of all four chambers. There is failure of
the tricuspid leaflets to coapt in systole (arrow). LV, left ventricle; RA, right atrium; RV, right ventricle.
A transverse plane spin-echo MRI in a young woman with arrhythmogenic right ventricular cardiomyopathy demonstrating a circumscribed area of enhanced
MR signal intensity in the right ventricular (RV) free wall (arrows) due to fatty infiltration.
Transverse short axis section through the ventricles from patients with cardiomyopathy. Upper left shows symmetrical left ventricular hypertrophy in
hypertrophic cardiomyopathy. Upper right shows dense white fibrous tissue obliterating the apex of both ventricles in endomyocardial fibrosis. Lower left shows a
globular, dilated left ventricle in a child with dilated cardiomyopathy. Lower right shows a grossly dilated right ventricle with adipose infiltration of the right ventricular
free wall in arrhythmogenic right ventricular dysplasia.
An echocardiogram (parasternal long axis view) of a patient with hypertrophic obstructive cardiomyopathy demonstrating hypertrophy of the interventricular
septum (IVS), enlargement of the left atrium (LA), and systolic anterior motion of the mitral valve, bringing it into contact with the septum (arrow).
Myocardial perfusion imaging may suggest septal ischemia in the presence of normal coronary arteries.
High troponin in first set of lab was highly indicative of myocarditis. During initial evaluation, the patient suddenly developed third degree heart block on the monitor but he remained asymptomatic
This young man came to the emergency department with 12 hours of continuing anterior chest pain. His pain was precipitated by exertion and movement. There was no significant pleuritic component. He is not a smoker and denied history of illicit drug or cocaine use. His CPK-MB and Troponin were both abnormal. The ECG shown above was the first one taken. At this point, he was having 10 of 10 chest pain with minimal relief from nitroglycerin and morphine. Fearing an Acute Myocardial Infarction (Heart Attack), the patient was taken emergently for cardiac catheterization. Fortunately, coronary arteriography showed normal coronary arteries without any evidence of atherosclerosis. His left ventricular function was abnormal and the left ventricular cavity appeared slightly dilated. His pain persisted, off and on, for the next 2-3 days. During this time, his cardiac enzymes continued to rise and the ECG abnormalities worsened. Five days later, echocardiography showed global left ventricular dysfunction.
The patient left the hospital with a diagnosis of Pericarditis/Myocarditis. Eight weeks later, his echocardiogram showed normal left ventricular function. His pain disappeared completely 96 hours after admission to the hospital.
Two-dimensional parasternal long-axis view depicting disproportionate thickening, increased echogenicity, and dyskinesis of the inferolateral wall relative to the septum; findings are consistent with tissue oedema.
Acute myocarditis in a 35-year old male presenting with acute chest pain, showing normal coronary arteries. Delayed enhancement MRI shows a strong subepicardial enhancement in the anterolateral LV wall as shown in the short-axis view (white arrows), b the spread in longitudinal direction can be well appreciated on the vertical long-axis view (white arrows)
Caption:Myocarditis. Light micrograph of human cardiac muscle with chronic myocarditis (inflammation). In this longitudinal section, muscle fibres run diagonally (purple). Abnormal features are a loss of organisation of the muscle fibres which are normally closely spaced, with the spaces between fibres (white, blue) representing oedema. There are neutrophils (white blood cells, purple dots) infiltrating the oedematous areas, as an early inflammatory response and to prevent infection. Chronic myocarditis is caused by rheumatic fever and virus infections, with enlargement of the heart. Magnification: x50 at 35mm size.