Direct-Current Shock for Atrial Fibrillation

Hollman, Arthur; Nicholson, H. Oliphant; Gray, IanR

doi:10.1016/s0140-6736(66)90401-6

Cited by 9 publications

(2 citation statements)

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“…A similar mechanism may follow the conversion of atrial fibrillation to sinus rhythm by quinidine (Broch and Miller, 1957), while Hollman and Nicholson (1966) have reported pulmonary oedema which followed the spontaneous reversion to sinus rhythm of paroxysmal atrial fibrillation which had lasted for five months. It is of interest that acute breathlessness occurred in only 2 of the 7 patients, and it is possible to be unaware of this particular complication unless chest x-rays are taken on the day after treatment.…”

Section: Discussionmentioning

confidence: 93%

Appraisal of electroconversion in treatment of cardiac dysrhythmias.

Resnekov¹,

McDonald²

1968

Heart

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and his colleagues (Lown, Amarasingham, and Neuman, 1962a;Lown et al., 1962b) described the experimental development and successful clinical use of direct-current shock for the conversion of atrial and ventricular dysrhythmias to sinus rhythm, which was soon confirmed by others (O'Brien, Resnekov, and McDonald, 1964;Oram et al., 1964;Morris et al., 1964). An analysis of the indications, results, and complications of the method is presented below; this is based on observations that have been made on 220 consecutive patients with atrial and ventricular dysrhythmias which were associated with a wide variety of underlying heart disease, and treated by direct-current shock. METHODSClinical and Laboratory. A careful history was taken from all patients before treatment, with particular note of the duration of the dysrhythmias, drug therapy, and past cardiac surgery. Patients were examined clinically before direct-current shock and on the day after it. Twelve-lead standard electrocardiograms were recorded, and if the nature of the dysrhythmia was still uncertain the effect of carotid sinus compression was noted, or additional leads, such as lead CR1 or an oesophageal lead, were recorded. Three chest radiographs were taken before and after treatment: a postero-anterior view, a lateral view (right), and a penetrated antero-posterior grid view at 122 cm. (40 in.) to indicate the size of the left atrium. The electrocardiogram and chest radiographs were repeated on the day after treatment, and sometimes on the second day after treatment if there had been a significant alteration in heart size after directcurrent shock. -The over-all size of the heart was estimated by the cardiothoracic ratio (Danzer, 1919), and the left atrium was graded from the penetrated antero-posterior grid view into normal (N), slight (+ 1),

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Section: Discussionmentioning

confidence: 93%

Appraisal of electroconversion in treatment of cardiac dysrhythmias.

Resnekov¹,

McDonald²

1968

Heart

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“…Any additional obstruction to flow across the mitral valve or left ventricular dysfunction would tend to aggravate the situation and result in the development of pulmonary oedema (Bell, 1966). Of particular interest are the accounts of Broch and Muller (1957) who demonstrated an increase in the pulmonary capillary pressure following the quinidine conversion of atrial fibrillation, and of Hollman and Nicholson (1966) who reported the onset of severe pulmonary cedema which followed the spontaneous reversion to sinus rhythm ofa 5-month episode of paroxysmal atrial fibrillation. Acute breathlessness occurred in only 2 of the 7 patients, so that this complication may be overlooked unless chest radiographs are taken on the day following DC shock.…”

Section: Discussionmentioning

confidence: 99%

Complications in 220 patients with cardiac dysrhythmias treated by phased direct current shock, and indications for electroconversion.

Resnekov¹,

McDonald²

1967

Heart

189

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Hemodynamic Changes After Cardioversion of Chronic Atrial Fibrillation

Upshaw¹

1997

Arch Intern Med

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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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Direct-Current Shock for Atrial Fibrillation

Cited by 9 publications

References 0 publications

Appraisal of electroconversion in treatment of cardiac dysrhythmias.

Appraisal of electroconversion in treatment of cardiac dysrhythmias.

Complications in 220 patients with cardiac dysrhythmias treated by phased direct current shock, and indications for electroconversion.

Hemodynamic Changes After Cardioversion of Chronic Atrial Fibrillation

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