After cardioversion of chronic atrial fibrillation to sinus rhythm, there is a gradual increase of 56% in cardiac output over 4 weeks. The increase is caused by the gradual return and increasing strength of left atrial mechanical activity as the atrial myopathy of chronic atrial fibrillation subsides. Cardiac output decreases after cardioversion of atrial fibrillation in more than a third of patients, and the decrease may last a week. Acute pulmonary edema is uncommon; 50% of cases occur within 3 hours of cardioversion, with a mortality of 18%. The reduced cardiac performance after cardioversion most likely results from the combination of heart disease and cardiac depressant effects of anesthetic drugs used. Pulmonary and/or coronary artery emboli and the resumption of right atrial mechanical activity before left atrial mechanical activity may be additional factors in the pathogenesis of pulmonary edema after cardioversion. Anticoagulant therapy should be continued for a month or longer after cardioversion in those patients who maintain sinus rhythm to prevent thromboembolism.

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Abstract-Why does the heart beat? This question-known as the myogenic versus neurogenic theory-dominated cardiac research in the 19th century. In 1839, Jan Evangelista Purkinje discovered gelatinous fibers in the ventricular subendocardium that he thought were muscular. Walter Gaskell, in 1886, demonstrated specialized muscle fibers joining the atria and ventricles that caused "block" when cut and found that the sinus venosus was the area of first excitation of the heart. By examining serial embryologic sections, Wilhelm His, Jr, showed that a connective tissue sheet became a bundle connecting the upper and lower cardiac chambers, the bundle of His. Sunao Tawara traced the atrioventricular (AV) bundle of His backward to find a compact node of fibers at the base of the atrial septum and forward where it connected with the bundles of cells discovered by Purkinje in 1839. Tawara concluded that this "AV connecting system" originated in the AV node, penetrated the septum as the His bundle, and then divided into left and right bundle branches that terminated in the Purkinje fibers. Martin Flack and Arthur Keith studied the conduction system of a mole and found a structure in the sinoauricular junction that histologically resembled the AV node. They felt that this was where "the dominating rhythm of the heart normally begins" and named it the sinoauricular node in 1907. The ECG of Einthoven soon brought a new understanding to the complex electrical system that makes the heart beat. In the second century, Claudius Galen observed that an excised, denervated heart continued to beat after isolation: "The heart, removed from the thorax, can be seen to move for a considerable time, . . . a definite indication that it does not need the nerves to perform its function." 5 William Harvey, in De Generatione Animalium (1651), stated that "the pulse has its origin in the blood. . .the cardiac auricle from which the pulsation starts, is excited by the blood." Albrecht von Haller, an experimental physiologist at the University of Göttingen, Germany, also postulated irritability of the heart muscle resulting from the intracardiac blood. On the basis of crushed spinal cord experiments in 1812, Cesar Legallois in France believed that the heartbeat was under nervous control. 2,3 In the 1830s and 1840s, the discovery of the sympathetic and parasympathetic nerves and ganglia inside and outside the heart, as well as the effect of galvanic stimulation on the nerves and heart, supported his nervous theory. 2,4 This ongoing, somewhat fevered, debate, arguing about whether the heartbeat was triggered by inherent excitation by the heart muscle itself or was due to an electrical stimulus from either external nervous or local ganglionic control, was known as the myogenic versus the neurogenic theory. 4 Ultimately, this physiological debate would be decided by anatomists who would discover the site of origin of the electrical impulse and its conducting pathway through the heart: first, the Purkinje fibers (1839); then, the bundle of His (1893); the...

Abstract-WoldemarMobitz, an early 20th century German internist, analyzed arrhythmias by graphing the relationship of changing atrial rates and premature beats to AV conduction. Through an astute mathematical approach, he was able to classify second-degree atrioventricular block into 2 types, subsequently referred to as Mobitz type I (Wenckebach) and Mobitz type II (Hay). Type I AV block was most often due to digitalis and was reversible. There were no associated pathological findings. Type II AV block frequently progressed to complete AV block and was associated with seizures, death, and pathological findings.