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English: 9-year-old girl with Ebstein's anomaly and Mahaim accessory pathway. ECGs recorded during sinus rhythm showing minimal pre-excitation, and during tachycardia (antedromic AVRT) showing maximal pre-excitation with LBBB morphology
Ebstein's anomaly is a congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced downwards towards the apex of the right ventricle of the heart. [1] EA has great anatomical heterogeneity that generates a wide spectrum of clinical features at presentation and is complicated by the fact that the ...
English: 12-lead ECG of a woman with Ebstein's anomaly (a congenital heart defect in which the opening of the tricuspid valve is displaced towards the apex of the right ventricle of the heart, resulting in a large right atrium). The ECG shows signs of right atrial enlargement, best seen in V1.
Figure 2: This image shows the three different types of aortic dissection. Figure 3: A visualization of the aorta (4) in relation to the pulmonary artery (5). Some examples of reported cardiovascular causes include: Congenital abnormalities: Atrial septal defect [5] Aortopulmonary window [5] Ebstein's Anomaly [6] Patent Ductus Arteriosus (PDA) [7]
Signs and symptoms depend on the specific type of defect. [3] Symptoms can vary from none to life-threatening. [7] When present, symptoms are variable and may include rapid breathing, bluish skin , poor weight gain, and feeling tired. [2] CHD does not cause chest pain. [2] Most congenital heart defects are not associated with other diseases. [3]
The severity of symptoms, and thus the likelihood of diagnosis, varies significantly depending on the amount of blood flow through the anomalous connections. In less severe cases, with smaller amounts of blood flow, diagnosis may be delayed until adulthood, when it can be confused with other causes of pulmonary hypertension. [ 5 ]
The condition is named after Wilhelm Ebstein and P. K. Pel who both published papers in 1887 noting the phenomenon. [5] [6] [7] Both doctors published in the same journal, though Pel published first by several months. A long-term dispute persisted between Pel and Ebstein on the etiology of the condition. [citation needed]
The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting. [5] In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide. [1]