MMW, Münchener medizinische Wochenschrift
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MMW Munch Med Wochenschr · Dec 1978
[Cardiogenic shock following acute myocardial infarction. Pathophysiology and clinical aspects (author's transl)].
The starting point of cardiogenic shock is an extensive myocardial infarction. Through a backward and forward failure of the left ventricle a shock-specific disturbance of the microcirculation occurs with a reduction of the circulation in the periphery of the body and development of a tissue acidosis (metabolic acidosis). Fall in blood pressure and cardiac volume, congestion of blood in the region of the pulmonary vessels and signs of reduced circulation in the body periphery (severe physical weakness, apathy, cold and clammy skin, oliguria) determine the clinical picture of cardiogenic shock. Therapeutically, intra-aortal balloon counter-pulsation, possibly combined with a cardiosurgical intervention, has reduced the mortality of cardiogenic shock after acute myocardial infarction from 90--100% to 60--70%.
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Electromyography reflects the anatomical situation in the muscle parenchyma. Changes in the anatomical structure are present if the normal potential form breaks up into small amplitude or even polyphasic potentials (myopathy type) or increases into high amplitude, broad and coarsely fragmented potentials (chronic neuropathy with regeneration). The caliber and type of muscle fibers are expressed in the speed of conduction. ⋯ Disturbances of neuromuscular transmission are detectable by direct stimulation of the muscle. Analysis of nerve conductivity permits the demonstration of diffuse (polyneuropathy type) or circumscribed (entrapment neuropathy type) nerve affections. The recording of the parameters mentioned is the domain of EMG.