Persistent Preload Defect in Severe Sepsis Despite Fluid Loading: Conclusion

21 Sep
2014

Persistent Preload Defect in Severe Sepsis Despite Fluid Loading: ConclusionMyocardial depression in sepsis in humans has been shown to result from circulatory myocardial depressant mediators. Participation of cardiac ischemia has been excluded by studies assessing coronary circulation during sepsis. The prognostic value of myocardial depression in sepsis appears controversial. Whereas a previous report related the risk of a fatal outcome from septic shock due to the intensity of myocardial depression, the present study found that LVEF did not predict outcome in individual patients. On the contrary, LVEF was initially lower in patients who recovered, as previously observed by others. A first explanation of this apparently paradoxical finding is that LVEF might not be a reliable index of LV systolic function in septic shock since the left ventricle is unloaded by the fall in systemic vascular resistance. Therefore, the finding of a normal or near-normal LVEF might just indicate depressed LV systolic function associated with an abnormally low resistive arterial compartment, with the potential risk of marked LVEF reduction when using vasopressor agents. More info

Associated with a less-depressed LV systolic function, we found a significantly smaller LVEDV in nonsurvivors than in survivors, as already reported by others. Moreover, despite fluid resuscitation, LV size continued to decrease during the monitoring period. In our opinion, this finding is suggestive of persistent fluid leak outside the vascular bed in the most severe cases, as has been suggested in septic patients. A recent study demonstrated that microvascular permeability was increased during sepsis. Thus, one can suggest a second explanation for the paradoxical relation between the intensity of LV systolic function impairment and the likelihood of recovery: reduced LVEF might represent an initially lifesaving process that limits cardiac output and related fluid leak across the vascular compartment. Other factors may also have contributed to preload reduction: reduced LV diastolic compliance resulting in filling impairment and also tachycardia, because LVEDV decreases linearly with increasing heart rate.
Some may object that the lack of pulmonary artery occlusion pressure (PAOP) monitoring in our study might have led to inadequate fluid resuscitation, thereby letting hypovolemia persist in our patients. In fact, most authors use PAOP as a target for fluid resuscitation. In recent years, however, repeated echocardiographic studies have established that PAOP measurement did not allow assessment of LV preload; at variance with others, we preferred CVP monitoring during fluid resuscitation. CVP provides a measure of the filling pressure for the whole heart. A target CVP value of 12 mm Hg was achieved in the present study by fluid resuscitation. Beyond this level, because the right heart is on the flat part of its function curve between 6 and 12 mm Hg, supplemental fluid therapy to reach a target PAOP unavoidably results in an excess fluid intake.
Be that as it may, prognosis of septic shock has not improved during the past 20 years despite a rational therapeutic approach, taking into consideration hemodynamic assessment by bedside right heart catheterization or echocardiography. The overall mortality (62%) in this study was quite similar to that reported in recent studies.’ Such poor results should prompt the search for a novel approach to the treatment of severe sepsis complicated by circulatory failure.

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