in the previous issue of critical care , huang and colleagues try to answer the unresolved question of the prognostic value of sepsis - related cardiomyopathy . since margaret parker and colleagues originally reported in 1984 that 65% of patients had significant left ventricular ( lv ) systolic dysfunction in the early phase of sepsis associated with acute lv dilatation ( > 100% increase in size ! ) and that such patients had a better prognosis , various groups have failed to replicate these results , leading to confusion and controversy .
the article by huang and colleagues is interesting because it reports a large meta - analysis including more than 700 septic patients available for lv analysis .
the meta - analysis failed to find any evidence for a protective effect of a decreased lv ejection fraction ( ef ) . nevertheless , the nonindexed lv dimension was moderately higher among survivors than nonsurvivors .
these results have to be interpreted with caution since in most studies included in the meta - analysis patients with lv systolic dysfunction received inotropic drugs . in the study by cariou and colleagues in 10 patients ,
most patients were infused with epinephrine or dobutamine . in the study performed by our group in 68 patients ,
bouferrache and colleagues reported recently that dobutamine significantly improves the macrocirculation in patients with a low flow state who show a 40% increase in cardiac output despite normal venous oxygen saturation .
de backer and colleagues demonstrated that the proportion of functional capillaries was decreased in septic patients compared with volunteers   and that dobutamine , by inducing a 21% increase in cardiac output , led to a nearly complete reversal of such alterations . in the study by rivers and colleagues , demonstrating a better prognosis in the early goal - directed therapy group , close to 14% of patients received dobutamine in the first 6 hours in the interventional group versus 0.8% in the control group .
finally , rhodes and colleagues , kumar and colleagues , and vallet and colleagues reported similar results - a huge decrease in mortality in septic patients who respond to dobutamine in terms of cardiac output [ 9 - 11 ] .
more interestingly , however , the article by huang and colleagues allows us to try to clarify the meaning of lv function in septic shock patients . a lot of confusion exists . in all experimental models of septic shock ,
lv contractility impairment - called septic cardiomyopathy - has been reported to be constant . in these studies , as in the study by barraud and colleagues , intrinsic contractility is assessed using a parameter that is not dependent on load conditions ; that is , systolic elastance .
unfortunately , this assessment requires the generation of pressure / volume loops , something difficult to achieve in human subjects at the bedside .
this difficulty is why in clinical practice most intensivists use lv systolic function parameters that are for the most part dependent on load conditions .
more than 20 years ago , robotham and colleagues nicely reiterated that lvef reflects the coupling between lv contractility and lv afterload .
in other words , a normal lvef may be observed when the arterial tone is severely depressed , despite seriously impaired intrinsic lv contractility .
everyone understands that it is crucial to remember this in septic shock , in which arterial tone is initially severely decreased .
lv systolic function , evaluated using an echocardiograph or another device , is more a reflection of arterial tone ( and its correction ) than of intrinsic lv contractility . in a 1990 study , jardin and
colleagues elegantly showed that patients with a normal lvef had a significantly lower systemic vascular resistance than patients with a low lvef in whom resistance was corrected .
as shown in figure 1 , it is then easy to understand that the incidence of lv systolic dysfunction greatly depends on the time of the evaluation .
this dependence only reflects the fact that , during resuscitation and treatment , vasoplegia and then lv afterload are corrected , thus unmasking septic cardiomyopathy .
h6 , h12 , h24 , h72 , the time ( hours ) between admission and echocardiographic evaluation . with these points in mind , we can revisit the results of margaret parker and colleagues ' study : it is not that the patients with a low ef survived better , but rather that the other patients had an increased mortality due to persistent profound vasoplegia .
this was suggested by our group in a study where 100% of patients with a hyperkinetic state ( lvef 67  7% ) finally died , compared with ' only ' 43% of patients with a hypokinetic state ( lvef 34  10% ) .
weng and colleagues showed recently that high peak systolic velocity measured at the mitral annulus by tissue doppler imaging might be associated with mortality in patients with septic shock , suggesting that profound vasoplegia inducing high contractility is linked to poor prognosis . in conclusion
, it will be very difficult to demonstrate that lv systolic dysfunction is associated with prognosis .
septic cardiomyopathy is constant and lv systolic function is more a reflection of the status of lv afterload .
rather , we have now to demonstrate what the best mortality - reducing strategy is when there is lv systolic dysfunction .
persistence of a hyperkinetic state is a warning signal suggesting that the septic process is not under control and that the patient has a high probability of dying .
 the meta - analysis of huang and coworkers failed to find any evidence for a protective effect of a decreased left ventricular ( lv ) ejection fraction ( ef ) . 
 these results have to be interpreted with caution since in most studies included in the meta - analysis patients with lv systolic dysfunction received inotropic drugs . 
 we have some arguments suggesting that such a treatment may improve macrocirculation and microcirculation and finally prognosis . 
 this paper allows us to clarify the meaning of lv function in septic shock patients . in all experimental models of septic shock using the load - independent parameter of lv systolic function , lv contractility impairment , called septic cardiomyopathy , has been reported to be constant . 
 however , lvef reflects the coupling between lv contractility and lv afterload . 
 a normal lvef may be observed when the arterial tone is severely depressed , as in septic shock , despite seriously impaired intrinsic lv contractility . 
 lv systolic function , evaluated using an echocardiograph or another device , is then more a reflection of arterial tone ( and its correction ) than of intrinsic lv contractility . as a consequence , 
 the incidence of lv systolic dysfunction greatly depends on the time of the evaluation , reflecting the fact that , during resuscitation and treatment , vasoplegia and then lv afterload are corrected , thus unmasking septic cardiomyopathy . with these points in mind , we can revisit the results of margaret parker 's original study : it is not that the patients with a low ef survived better , but rather that the other patients had an increased mortality due to persistent profound vasoplegia . 
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