[Physiopathology of myocardial dysfunction in septic shock]

Left ventricular dysfunction is rarely a prominent feature of septic shock. Initially, it is masked by circulatory changes and adaptive phenomena which increase the cardiac output. Evaluation of intrinsic myocardial function is therefore difficult in this pathology. The different experimental models used (cell culture, isolated muscle, isolated perfused heart and whole animal) and recent clinical studies using angiographic, catheter and echocardiographic data, have confirmed that this condition exists. Its physiopathology is not yet fully understood and involves several mediators. The direct effect of bacterial endotoxins has not been formally established. However, therapy with anti-endotoxin antibodies does give encouraging results. The cytokines, such as interleukin-1, tumour necrosis factor, and platelet activating factor play a key role between the infectious factors and cellular mediators. Their effects on the myocardium are subject of much on-going research. Current date, in particular with respect to the tumour necrosis factor, suggest that they may have a direct cardiodepressor factor. The presence of a circulating negative inotropic substance has been suspected for many years. Recent studies tend to confirm this hypothesis though the substance itself has not yet been isolated. The theory of reduced coronary flow causing myocardial dysfunction in septic shock has fallen out of favour. Some experimental evidence supports the clinical impression of reduced vascular and cardiac reactivity to catecholaminergic stimulation. The actions of different membrane structures involved have not been determined. At cellular level, changes in calcium metabolism, which regulates muscle contraction and relaxation, probably play an important role in septic shock. In addition to the symptomatic therapeutic advances that have been made in septic shock, specific myocardial treatment could be beneficial.