Sepsis-induced cardiomyopathy

Abstract

Myocardial dysfunction is one of the main predictors of poor outcome in septic patients, with mortality rates next to 70%. During the sepsis-induced myocardial dysfunction, both ventricles can dilate and diminish its ejection fraction, having less response to fluid resuscitation and catecholamines, but typically is assumed to be reversible within 7-10 days. In the last 30 years, It's being subject of substantial research; however no explanation of its etiopathogenesis or effective treatment have been proved yet. The aim of this manuscript is to review on the most relevant aspects of the sepsis-induced myocardial dysfunction, discuss its clinical presentation, pathophysiology, etiopathogenesis, diagnostic tools and therapeutic strategies proposed in recent years.

Fig. (1)

Echocardiographic image of a patient in septic shock secondary to fecaloid peritonitis. The left ventricle shows a pathological remodeling similar to that generated in an anterior wall acute myocardial infarction.

Fig. (2)

Transesophageal image projection which displays the left ventricle of a 18-year-old female patient with urinary sepsis by E. colli. The arrow points to "ballooning" septoapical segment.

Fig. (3)

Transesophageal image projection which shows the pulmonary veins flow. Quantifying the systolic filling fraction, left atrial pressure can be calculated. (LA: Left atria. LV: Left ventricle. LAp: left atrial appendage).

Fig. (4)

Left ventricular segmental contractility alterations. Evaluation by quantitative tecniques based on tissue Doppler image (a), or the velocity vector analysis (b).

Fig. (5)

Stroke volume echocardiographic calculus: According to the equation SV= π x r² x VTI_LVOT = 59 ml (Normal). (SV= systolic volume, VTI_LVOT= Left ventricular outflow tract velocity-time integral, r = left ventricular outflow tract ratio).