It is important to recognize that the original definitions relied only on the degree of vasodilatation, whereas in the modification by both the International Sepsis Definition Conference and Annane et al2 myocardial depression defined as low cardiac index or echocardiographic evidence of cardiac dysfunction has been included in the definition of severe sepsis (Table 1).
Abnormalities of cardiac function are quite common in patients with sepsis. The prevalence of this transient phenomenon critically depends on the population studied, the definition applied, and the time point during the course of the disease. Approximately 50% of patients with severe sepsis and septic shock seem to have any form of impairment of left ventricular systolic function.” Reading here
The phenomenon of myocardial depression is mediated by circulating depressant substances, which until now have been incompletely characterized. Among those on a list of possible candidates, tumor necrosis factor-а and interleukin-1p play a central role. In addition, interleukin-6 has been shown to be a key mediator of myocardial dysfunction in children with meningococcal septic shock. A comprehensive discussion of the numerous pathways involved in the complex pathogenesis of sepsis is beyond the aim of the present clinically oriented review, but can be found elsewhere.
The hemodynamic pattern in human septic shock is generally characterized by a hypercirculatory state including decreased systemic vascular resistance and a markedly increased cardiac index after adequate fluid resuscitation. Nevertheless, several studies have revealed clear evidence of intrinsic depressed left ventricular performance in patients with septic shock. The phenomenon of “myocardial depression” was first described by Parker and coworkers, who performed serial radionuclide ventriculograms in 20 patients with septic shock, 7 of whom died during their stay in the ICU. Ten of 13 survivors had a reversibly depressed left ventricular ejection fraction (LVEF) of < 0.4, whereas none of the nonsurvivors had an LVEF of < 0.4. Survivors had substantially increased left ventricular end-diastolic and end-systolic volumes, and, thus, preserved stroke volumes despite impaired LVEF, whereas in nonsurvivors ventricular dimensions remained normal.
Table 1—Definitions of SIRS and Different Degrees of Severity of Sepsis
|SIRS||Two or more of the following conditions: temperature > 38.5°C or < 35.0°C; heart rate of > 90 beats/min; respiratory rate of > 20 breaths/min or PacO£ of < 32 mm Hg; and WBC count of > 12,000 cells/mL,< 4,000 cells/mL, or > 10% immature (band) forms|
|Sepsis||SIRS in response to documented infection (culture or Gram stain of blood, sputum, urine, or normally sterile body fluid positive for pathogenic microorganism; or focus of infection identified by visual inspection, eg, ruptured bowel with free air or bowel contents found in abdomen at surgery, wound with purulent discharge)|
|Severe sepsis||Sepsis and at least one of the following signs of organ hypoperfusion or organ dysfunction: areas of mottled skin; capillary refilling of > 3 s; urinary output of < 0.5 mL/kg for at least 1 h or renal replacement therapy; lactate > 2 mmol/L; abrupt change in mental status or abnormal EEG findings; platelet count of < 100,000 cells/mL or disseminated intravascular coagulation; acute lung injury/ARDS; and cardiac dysfunction (echocardiography)|
|Septic shock||Severe sepsis and one of the following conditions: systemic mean BP of < 60 mm Hg (< 80 mm Hg if previous hypertension) after 20-30 mL/kg starch or 40-60 mL/kg serum saline solution, or PCWP between 12 and 20 mm Hg; and need for dopamine of < 5 ^g/kg/min, or norepinephrine or epinephrine of < 0.25 ^g/kg/min to maintain mean BP at > 60 mm Hg (80 mm Hg if previous hypertension)|
|Refractory septic shock||Need for dopamine at > 15 ^g/kg/min, or norepinephrine or epinephrine at > 0.25 ^g/kg/min to maintain mean BP at > 60 mm Hg (80 mm Hg if previous hypertension)|