PHYSIOPATHOLOGY OF MYOCARDIAL DYSFUNCTION DURING SEPTIC SHOCK

Left ventricular dysfunction is rarely a prominent feature of septic s hock. Initially, it is masked by circulatory changes and adaptive phen omena which increase the cardiac output. Evaluation of intrinsic myoca rdial function is therefore difficult in this pathology. The different experimental models used (cell culture, isolated muscle, isolated per fused heart and whole animal) and recent clinical studies using angiog raphic, 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-endotoxi n antibodies does give encouraging results. The cytokines, such as int erleukin-1, tumour necrosis factor, and platelet activating factor pla y a key role between the infectious factors and cellular mediators. Th eir effects on the myocardium are subject of much on-going research. C urrent date, in particular with respect to the tumour necrosis factor, suggest that they may have a direct cardiodepressor factor. The prese nce of a circulating negative inotropic substance has been suspected f or many years. Recent studies tend to confirm this hypothesis though t he substance itself has not yet been isolated. The theory of reduced c oronary flow causing myocardial dysfunction in septic shock has fallen out of favour. Some experimental evidence supports the clinical impre ssion of reduced vascular and cardiac reactivity to catecholaminergic stimulation. The actions of different membrane structures involved hav e not been determined. At cellular level, changes in calcium metabolis m. which regulates muscle contraction and relaxation, probably play an important role in septic shock. In addition to the symptomatic therap eutic advances that have been made in septic shock, specific myocardia l treatment could be beneficial.