Document Detail


Diffuse left ventricular hypokinesis in cardiogenic shock--its cause or consequence?
MedLine Citation:
PMID:  6723316     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Five patients in cardiogenic shock due to acute myocardial infarction were examined by two-dimensional echocardiography. In one patient, cardiogenic shock developed only after rupture of the interventricular septum, four subjects had "primary" cardiogenic shock. In these four persons there were found extensive disturbances of left ventricular wall motion (the mean extent of the akinetic or dyskinetic zone amounted to 41% of the left ventricle (LV). However, equally extensive (and even larger) disturbances of LV kinetics were found in another 11 patients with acute MI, in whom there did not develop cardiogenic shock. The basic difference between the two groups consisted in the fact that in patients in cardiogenic shock the remaining part of the left ventricle exhibited severe hypokinesis, whereas in other infarcts it was normokinetic or hyperkinetic. Autopsy findings in all patients revealed severe diffuse involvement of all coronary arteries. In the discussion, it is pointed out that the above-mentioned phenomenon (hypokinesis of the "intact" part of the left ventricle) may be both one of the causes of shock as well as merely its consequence.
Authors:
P Widimský; P Gregor; V Cervenka; V Vísek
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cor et vasa     Volume:  26     ISSN:  0010-8650     ISO Abbreviation:  Cor Vasa     Publication Date:  1984  
Date Detail:
Created Date:  1984-07-11     Completed Date:  1984-07-11     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0372614     Medline TA:  Cor Vasa     Country:  CZECHOSLOVAKIA    
Other Details:
Languages:  eng     Pagination:  27-31     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Echocardiography*
Heart Ventricles / physiopathology*
Humans
Myocardial Contraction
Myocardial Infarction / complications
Shock, Cardiogenic / etiology,  physiopathology*

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