Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection and is associated with a high mortality rate in the ICU. Sepsis induced cardiomyopathy (SICM) is a multi-factorial process that appears in approximately 50% of patients with sepsis/septic shock and is associated with increased mortality. It is suggested that ketone bodies are more efficient substrates of energy metabolism than glucose, with a lower oxygen consumption per ATP-molecule produced and that the failing human heart increases the capacity to metabolize ketones. Previous studies have found acute beneficial hemodynamic effects of ketone esters in patients with chronic heart failure and cardiogenic shock, respectively. Improved hemodynamics and reduced systemic oxygen consumption as an effect of ketone esters might be of great benefit in patients admitted to the ICU. Thus, the investigators aim to investigate the hemodynamic effects of ketone esters in patients with sepsis induced cardiomyopathy in this randomized, placebo-controlled, double-blinded, cross-over, acute intervention study. .
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
TRIPLE
Enrollment
12
Ketone ester: 3-hydroxybutyrate as enteral bolus (500 mg/kg)
Maltodextrin (isovolumic and isocaloric placebo) as enteral bolus
Global longitudinal strain
Echocardiographic measure obtained from transthoracic echocardiography
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
Left ventricular ejection fraction
Echocardiographic measure obtained from transthoracic echocardiography
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
Mean arterial pressure
Obtained from invasive blood pressure measurement (arterial line)
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
Cardiac output
Obtained from transthoracic echocardiography
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
Peripheral blood oxygen saturation
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
Arterial blood pH
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
Arterial blood lactate
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
Accumulated norepinephrine
Time frame: From intervention to 3 hours after intervention (this is assessed for both treatment arms)
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