Myocardial failure.
The majority of evidence suggests that there is myocardial dysfunction resulting from sepsis. Clinical observations seem to suggest that the dysfunction is not on the basis of decreased venous return of increased afterload. Reduced myocardial compliance and isolated right ventricular failure also do not account for what is seen clinically. The explanation appears to be decreased myocardial contractility. Several factors may be responsible for reducing contractility, including altered response to catecholamines; metabolic acidosis; altered distribution of blood flow within the myocardial wall resulting in hypoxic regions; the elaboration of substances that act directly to reduce contractility, including intestinal shock factors and endorphins; and alterations of excitation-contraction coupling resulting from changes in calcium concentrations or reduced responsiveness to the calcium ion. Further work is needed to determine which of these factors predominate.
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000502:physiology; D002118:Calcium / Q000097:blood; D002302:Cardiac Output; D002395:Catecholamines / Q000097:blood; D004285:Dogs; D006323:Heart Arrest / Q000209:etiology* / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D000860:Hypoxia / Q000150:complications; D009200:Myocardial Contraction; D012772:Shock, Septic / Q000150:complications* / Q000503:physiopathology
D000889:Anti-Arrhythmia Agents; D002395:Catecholamines; D002118:Calcium