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Biomedical subjects

C B Upshaw

Publications and source records attributed to C B Upshaw.

18 recordsLinked to original sources
PubMed2001

Alfred Lewis Galabin and the first human documentation of atrioventricular block.

Using an apexcardiogram, Galabin was the first person to document atrioventricular (AV) block in humans. He performed his studies while working as a house officer at Guy's Hospital, London, United Kingdom. His patient was 34 years old, experienced attacks of near syncope, and had a pulse rate that varied between 25 and 30 beats/min. A laddergram of the patient's apexcardiogram suggests advanced AV block with 3 to 1 and 2 to 1 AV conduction with Wenckebach periodicity. We review the history of AV block beginning with the introduction of graphic recordings in 1847 by Ludwig, and include the contributions of Stannius, Luciani, Gaskell, Wenckebach, Hay, and Mobitz. Although he is little known today among cardiovascular physicians, we recognize Galabin as the first person to demonstrate AV block in humans.

Heart Block↗
PubMed2000

Luigi Luciani and the earliest graphic demonstration of Wenckebach periodicity.

Using an isolated frog heart preparation with ligatures around the atria, Luigi Luciani, an Italian physiologist working in 1873 in Carl Ludwig's famous laboratory in Leipzig, was the first to demonstrate cardiac group beating, which he named periodic rhythm. He attributed this to increased resistance to impulse propagation between the atria and the ventricle. Karel F. Wenckebach, in his 1899 landmark report of group beating in a patient in which he also used pulse tracings, credited Luciani with this discovery. Wenckebach referred to the phenomena as "Luciani periods." With the advent of electrocardiography in the early 20th century, this form of group beating became known as Wenckebach periodicity and then as Mobitz type I atrioventricular block. We reanalyzed Luciani's original paper and pulse tracings, and we show that periodic rhythm does indeed meet the criteria of second-degree atrioventricular block as established by Wenckebach. We also reviewed the career of Luciani, who was an important investigator, outstanding teacher and mentor, and distinguished leader of 19th-century physiology. We conclude that Wenckebach still deserves to have his name eponymously attached to this type of atrioventricular block because he was the first to unravel the complicated relationship between atrial and ventricular conduction.

Animals↗
PubMed1999

The Wenckebach phenomenon: a salute and comment on the centennial of its original description.

In 1899, Karel F. Wenckebach unraveled the complicated arrhythmia that bears his name--one of the most famous eponyms in medicine. He reported his findings before the benefit of clinical electrocardiography or the discovery of the sinoatrial and atrioventricular nodes. Born and educated in The Netherlands, Wenckebach first worked in Utrecht in the physiology laboratory of T.W. Engelmann, his respected mentor, where he became familiar with kymographic recordings and rhythm disturbances in frog experiments. He then entered country practice in 1891, where he gained great respect for practicing physicians as well as the importance of clinical experience. In 1896, he returned to Utrecht to work again in the laboratory with Engelmann. In 1898, a woman consulted Wenckebach about her irregular pulse. His investigation of her irregular heart action by using radial arterial pulse tracings and experimental atrial and ventricular pulse tracings from the heart of a frog enabled him to discover the mechanism of partial heart block. In later years, he continued to be a leader in academic medicine, chairing the departments of medicine in Groningen, Strasbourg, and Vienna. He achieved fame for investigating cardiac arrhythmias and other contributions and is considered to be one of the founders of modern cardiology. He is remembered for his insight into atrioventricular conduction, which is as valid today as it was a century ago.

Female↗
PubMed1997

Hemodynamic changes after cardioversion of chronic atrial fibrillation.

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.

Anesthetics↗
PubMed1993

Seeing through the maze of complete left bundle branch block.

LBBB obscures many cardiovascular diagnoses, but it is now possible to diagnose LVH and MI in the presence of LBBB. It is possible from accumulated data to synthesize a new clinical entity: The Complete Left Bundle Branch Block Syndrome. This encompasses the following: Uncomplicated LBBB: (1) the abnormal ECG configuration with normal QRS axis; (2) reversed splitting of the cardiac second sound due to delay of aortic valve closure; (3) significant left ventricular systolic and diastolic dysfunction due to the abnormal sequence of left ventricular activation and relaxation; (4) ventricular septal hypokinesis, and during thallium stress testing ventricular septal perfusion defects which tend to invalidate the results of the test; (5) the vast majority of patients with LBBB have organic heart disease, but 16% have structurally normal hearts except for the conduction system disease; Complicated LBBB: (6) left or right axis deviation or QRS duration greater than 0.14 secs. indicates a greater degree of left ventricular disease and dysfunction than LBBB alone and nearly excludes the presence of conduction disease only; (7) disordered function of the SA node, AV node and right bundle branch.

Bundle of His↗
PubMed1980

Retrograde Wenckebach phenomenon induced by right ventricular pacing.

Retrograde Wenckebach phenomenon, occurring between the paced ventricles and the atria, developed in a patient with acute anterior myocardial infarction and ventricular dysfunction. This report has summarized previous investigations on ventriculoatrial conduction and their application to this case. With paced ventricular beats, VA conduction may occur but VA conduction time is longer than AV conduction time at similar heart rates. Progressive degrees of VA block develop at the AV node as the heart rate speeds. VA conduction may occur in the presence of complete AV block. Concealed VA conduction to the AV node supresses AV conduction.

Electrocardiography↗
PubMed1979

Noncirrhotic portal hypertension after arsenic ingestion.

Five years after arsenic therapy, the patient described had noncirrhotic portal hypertension, for which he had splenectomy and anastomosis of the splenic vein to the left renal vein. During the 12-year postoperative period he had Bowen's disease (skin carcinoma), but has had normal liver function and no further gastrointestinal bleeding. Arsenic exposure in humans is common throughout the world and may lead to late complications such as noncirrhotic portal hypertension and skin carcinoma, as well as malignancies of the lungs, liver, and lymphatic systems. It may also lead to severe arteriosclerosis with involvement of the heart and extremities.

Arsenic↗
PubMed1975

Precordial honk due to tricuspid regurgitation.

A systolic honk developed in a woman with idiopathic cardiomyopathy and congestive heart failure. The honk was present only during deep inspiration, disappeared as her cardiovascular status improved, but recurred when her cardiovascular function declined. Further investigation indicated that the honk was the result of tricuspid regurgitation.

Cardiac Catheterization↗