Myocardial Dysfunction in Severe Sepsis

Abstract

Septic shock is one of the main causes of admission and death in critically ill patients. Septic shock is a combination of hypovolemia, peripheral vascular dysfunction resulting in hypotension and abnormalities in the local/regional distribution of blood flow, cardiac failure, and cell dysfunction. Importantly, the hemodynamic profile differs from patient to patient, at least regarding the macrocirculatory disturbances. Some septic patients experience a high degree of hypovolemia, whereas others experience a high degree of impairment of vascular tone, and still others experience severe cardiac failure. A variety of combinations can thus exist. Using trans esophageal echocardiography (TEE), recently showed that global left ventricular (LV) hypokinesia, defined by left ventricle ejection fraction (LVEF) <45%, was observed in 60% of patients during the first 3 days of treatment of septic shock. In 39% of patients, left ventricular hypokinesia was present at admission (primary hypokinesia), and in 21% of patients, left ventricle ejection fraction was normal at admission and left ventricular hypokinesia appeared after norepinephrine infusion (secondary hypokinesia). Myocardial depression in patients with septic shock was initially described as biventricular dilatation associated with a depressed left ventricle ejection fraction, which was transient and reversible with a gradual return toward a normal ventricular volume and normal ejection fraction in 7 to 10 days after onset of sepsis. There is still some controversy on the presence of acute left ventricle dilatation in septic shock. Some echocardiographic studies reported a left ventricle dilatation associated with left ventricle systolic impairment in animals and humans with septic shock, whereas the left ventricle was not dilated in other studies. Numerous mechanisms have been suspected to be responsible for the sepsis-induced cardiac dysfunction. It is now admitted that ischemic phenomena do not play a major role in sepsis-induced cardiac dysfunction. Coronary blood flow was shown to be preserved in patients with septic shock. Nevertheless, if diastolic arterial pressure is very low because of a marked decrease in vascular tone, myocardial ischemia could ensue because diastolic blood pressure is the driving pressure for the LV coronary blood flow. Cytokines such as interleukin 1 (IL-1) and tumor necrosis factor alpha (TNFα) are thought to be the circulating myocardial depressant factors. However, although cytokines might account for myocardial depression at the initial phase of sepsis, they cannot exert a prolonged effect because interleukin 1 IL-1 and tumor necrosis factor alpha TNFα plasma levels return to normal values within 48 hours after the sepsis onset. Moreover, studies using isolated cardiomyocytes harvested from endotoxin-induced septic animals, reported contractile depression similar to in vivo measurements in spite of the absence of a direct contact with plasma. This suggests that intramyocardial mechanisms can be involved in the sepsis-induced cardiac dysfunction irrespective of the presence of circulating depressing substances. Echocardiography is the reference method with which to evidence sepsis-induced cardiac dysfunction. Echocardiography allows measuring the left ventricle ejection fraction LVEF, which is the key variable for diagnosing myocardial depression .Pulmonary artery catheterization (PAC) is a traditional hemodynamic monitoring method in patients with septic shock. It can help to detect sepsis-induced cardiac dysfunction by showing low cardiac output and elevated cardiac filling pressures.