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Clinical review: Myocardial depression in sepsis and septic shock.

Court O, Kumar A, Parrillo JE, Kumar A - Crit Care (2002)

Bottom Line: Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with severe sepsis and septic shock.Cardiac function usually recovers within 7-10 days in survivors.Myocardial dysfunction does not appear to be due to myocardial hypoperfusion but due to circulating depressant factors, including the cytokines tumor necrosis factor alpha and IL-1beta.

View Article: PubMed Central - PubMed

Affiliation: Section of Critical Care Medicine, Health Sciences Center, University of Manitoba, Winnipeg, Canada.

ABSTRACT
Myocardial dysfunction frequently accompanies severe sepsis and septic shock. Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with severe sepsis and septic shock. Myocardial depression exists despite a fluid resuscitation-dependent hyperdynamic state that typically persists in septic shock patients until death or recovery. Cardiac function usually recovers within 7-10 days in survivors. Myocardial dysfunction does not appear to be due to myocardial hypoperfusion but due to circulating depressant factors, including the cytokines tumor necrosis factor alpha and IL-1beta. At a cellular level, reduced myocardial contractility seems to be induced by both nitric oxide-dependent and nitric oxide-independent mechanisms. The present paper reviews both the clinical manifestations and the molecular/cellular mechanisms of sepsis-induced myocardial depression.

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The effect of serum from septic shock patients and control groups on the extent of myocardial cell shortening of spontaneously beating rat heart cells in vitro. Septic shock patients during the acute phase demonstrated a statistically significant lower extent of shortening (P < 0.001) compared with any other group. Reproduced with permission from [38].
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Figure 6: The effect of serum from septic shock patients and control groups on the extent of myocardial cell shortening of spontaneously beating rat heart cells in vitro. Septic shock patients during the acute phase demonstrated a statistically significant lower extent of shortening (P < 0.001) compared with any other group. Reproduced with permission from [38].

Mentions: The first study to actually show a link between septic shock-associated myocardial depression in humans with the myocyte depressant effects of a patient's own septic serum was carried out by Parrillo et al. in 1985 [38]. Serum from patients with septic shock generated a significant concentration-dependent depression of in vitro myocyte contractility (Fig. 6). The investigators were also able to demonstrate a strong correlation between the timing and degree of septic shock-associated decrease in LVEF in vivo and cardiac myocyte depression in vitro induced by exposure to serum from the same patients.


Clinical review: Myocardial depression in sepsis and septic shock.

Court O, Kumar A, Parrillo JE, Kumar A - Crit Care (2002)

The effect of serum from septic shock patients and control groups on the extent of myocardial cell shortening of spontaneously beating rat heart cells in vitro. Septic shock patients during the acute phase demonstrated a statistically significant lower extent of shortening (P < 0.001) compared with any other group. Reproduced with permission from [38].
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC153435&req=5

Figure 6: The effect of serum from septic shock patients and control groups on the extent of myocardial cell shortening of spontaneously beating rat heart cells in vitro. Septic shock patients during the acute phase demonstrated a statistically significant lower extent of shortening (P < 0.001) compared with any other group. Reproduced with permission from [38].
Mentions: The first study to actually show a link between septic shock-associated myocardial depression in humans with the myocyte depressant effects of a patient's own septic serum was carried out by Parrillo et al. in 1985 [38]. Serum from patients with septic shock generated a significant concentration-dependent depression of in vitro myocyte contractility (Fig. 6). The investigators were also able to demonstrate a strong correlation between the timing and degree of septic shock-associated decrease in LVEF in vivo and cardiac myocyte depression in vitro induced by exposure to serum from the same patients.

Bottom Line: Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with severe sepsis and septic shock.Cardiac function usually recovers within 7-10 days in survivors.Myocardial dysfunction does not appear to be due to myocardial hypoperfusion but due to circulating depressant factors, including the cytokines tumor necrosis factor alpha and IL-1beta.

View Article: PubMed Central - PubMed

Affiliation: Section of Critical Care Medicine, Health Sciences Center, University of Manitoba, Winnipeg, Canada.

ABSTRACT
Myocardial dysfunction frequently accompanies severe sepsis and septic shock. Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with severe sepsis and septic shock. Myocardial depression exists despite a fluid resuscitation-dependent hyperdynamic state that typically persists in septic shock patients until death or recovery. Cardiac function usually recovers within 7-10 days in survivors. Myocardial dysfunction does not appear to be due to myocardial hypoperfusion but due to circulating depressant factors, including the cytokines tumor necrosis factor alpha and IL-1beta. At a cellular level, reduced myocardial contractility seems to be induced by both nitric oxide-dependent and nitric oxide-independent mechanisms. The present paper reviews both the clinical manifestations and the molecular/cellular mechanisms of sepsis-induced myocardial depression.

Show MeSH
Related in: MedlinePlus