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can -blockers improve outcomes in septic patients with myocardial depression ? in the previous issue of critical care , schmittinger and colleagues   discuss the results of treating myocardial depression in septic shock patients with the combination of milrinone and metoprolol .
support included volume infusion , treatment with milrinone ( a phosphodiesterase inhibitor ) and rapid addition of norepinephrine then vasopressin ( 31 of 40 patients ) based on hemodynamic measurements .
metoprolol , a 1-selective adrenergic antagonist , was given enterally at low doses ( 25 to 47.5 mg / day ) .
over 96 hours of follow - up , inotropic and vasopressor doses decreased , heart rate decreased , and cardiac output remained stable .
specifically , on metoprolol , norepinephrine and milrinone dosages had to be increased in 22.5% and 15% of patients , respectively .
dialysis makes interpreting creatinine changes difficult and the use of a linear mixed effects model for analysis can lead to less accurate type 1 error rates in small sample sizes . despite these limitations ,
this is one of the first trials to suggest the feasibility of acutely treating myocardial depression from sepsis with adrenergic antagonists . despite advances in the care of septic patients
myocardial injury and depression are common during sepsis and are likely multi - factorial in etiology .
the adrenergic nervous system is activated in sepsis and pharmacological doses of -agonists are commonly utilized during goal directed therapy to support oxygen delivery and maintain perfusion pressure .
there is a large body of evidence suggesting that excessive adrenergic levels can cause myocardial damage .
transgenic animals with overexpression of genes involving adrenergic signaling develop myocardial apoptosis , fibrosis , contractile dysfunction and eventually left ventricular dilatation . in cell culture , catecholamines have been shown to cause myocardial cell death and induce maladaptive changes in gene expression .
severe head injury causes massive adrenergic discharge resulting in myocardial necrosis and cardiac dysfunction . in chronic heart failure ,
activation of the adrenergic nervous system is associated with increased mortality , and inotropic therapy worsens outcomes .
in general -blockers are well tolerated even in severe heart failure when started at a low dose .
recent large prospective trials would mandate caution when using -blockers in acute settings of hemodynamic compromise .
the commit trial in acute myocardial infarction showed that metoprolol 's benefit in reducing reinfarction and arrhythmia ( 10 per 1,000 ) was offset by an increase in cardiogenic shock ( 11 per 1,000 ) .
this was most prominent in the first day of therapy in elderly patients with tachycardia and low blood pressure , a population reminiscent of the one discussed in the current series .
the poise trial showed that metoprolol , started 2 to 4 hours before surgery in high risk cardiac patients , led to increased rates of death and stroke .
myocardial depression with -blockers could explain the need to escalate therapy with vasoactive drugs in the current series .
gore and colleagues   showed that esmolol acutely reduced cardiac output by 20% in septic patients .
they found that even 6.25 mg of metoprolol , given orally , acutely decreased cardiac output , stroke volume and stroke work index .
after 3 months and uptitration to 50 mg bid , the administration of the drug continued to cause a decrease in cardiac output and stroke work index .
the use of inotropes to bridge patients to -blockade has only been reported in small heart failure studies .
based on the above safety concerns , this strategy should be considered experimental until further randomized controlled studies are conducted . the reported incidence of hypotension and decreased cardiac output is high enough that it might cancel the potential metabolic and anti - adrenergic benefits of metoprolol .
the likelihood that the changes observed in hemodynamic parameters are not due to metoprolol is high .
if further studies are planned , smaller doses of metoprolol should be considered in dose ranging trials .
carvedilol and nebivolol have vasodilatory properties that could precipitate vascular collapse in this patient population .
non - selective -blockers such as esmolol and propranolol may withdraw excessive adrenergic support and precipitate worsening myocardial function .
sepsis with myocardial dysfunction is seen commonly . 
 beta - blockers have been used successfully to treat chronic heart failure based on the premise that chronically elevated adrenergic drive is detrimental to the myocardium . 
 however , recent reports on the acute use of beta - blockers in situations with potential hemodynamic compromise have shown the risks associated with this approach . in critical situations , the main effect of adrenergic activation is to support cardiovascular function . 
 caution should be exercised in designing studies to assess beta - blockers in septic patients .