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Sepsis-Induced Cardiac Dysfunction

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Information about Sepsis-Induced Cardiac Dysfunction

Published on July 19, 2007

Author: shivabirdi

Source: slideshare.net

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Mechanism of Sepsis-induced cardiac dysfunction Ricardo Riveros M.D. Cleveland Clinic CCM 2007 Vol. 35,N. 6

Objetives To provide a detailed overview on sepsis-induced cardiac dysfunction in general and on intrinsic myocardial depression in particular.

To provide a detailed overview on sepsis-induced cardiac dysfunction in general and on intrinsic myocardial depression in particular.

Patient Studies Frequency remains unknown. No consensus exist for a suitable definition. Survivors from septic shock have lower EF and higher end-diastolic volumes compared with nonsurvivors (protective role). The decrease in EF is reversible

Frequency remains unknown.

No consensus exist for a suitable definition.

Survivors from septic shock have lower EF and higher end-diastolic volumes compared with nonsurvivors (protective role).

The decrease in EF is reversible

Patient Studies. By Echocardiography: Initial Hyperdynamic LV function during initial resucitation is an independent predictor of sepsis. In septic shock Low EF with High Lv end diastolic volume

By Echocardiography: Initial Hyperdynamic LV function during initial resucitation is an independent predictor of sepsis.

In septic shock Low EF with High Lv end diastolic volume

Patient Studies BIOMARKERS: Troponins I- T: elevated in 31-85%. Associated with higher catecolamines requirement, lower stroke work index, LVEF and higher mortality. BNP: Afected by age, renal function,gender. High levels are correlated with adverse otcomes

BIOMARKERS:

Troponins I- T: elevated in 31-85%. Associated with higher catecolamines requirement, lower stroke work index, LVEF and higher mortality.

BNP: Afected by age, renal function,gender. High levels are correlated with adverse otcomes

Animal Models Variability on LV assessment, type and duration of insult, species,duration of study, volume resucitation, anesthesia: The physiologic and immunologic response will vary and will affect outcome

Variability on LV assessment, type and duration of insult, species,duration of study, volume resucitation, anesthesia:

The physiologic and immunologic response will vary and will affect outcome

 

Circulatory and microvascular Intravascular volume depletion- underfilling on the heart- reduced cardiac output - oxygen supply-demand imbalance. Myocardial edema, pulmonary HTN, Intrinsic cardiac contractility Endothelial Cell activation: Nitric oxide (Isometric contraction), endotelin and prostaglandins

Intravascular volume depletion- underfilling on the heart- reduced cardiac output - oxygen supply-demand imbalance.

Myocardial edema, pulmonary HTN, Intrinsic cardiac contractility

Endothelial Cell activation: Nitric oxide (Isometric contraction), endotelin and prostaglandins

Autonomic dysregulation Apoptosis in cardiovascular autonomic centers. Tachycardia: Restricted diastolic filling, increase oxygen requirement, cardiomyopathy

Apoptosis in cardiovascular autonomic centers.

Tachycardia: Restricted diastolic filling, increase oxygen requirement, cardiomyopathy

Metabolic Changes Increase lactate extraction, decrease ketones, fatty acids and glucose intake. Septic patients with organ dysfunction can tolerate lower values of oxygen delivery but also reduce cellular oxygen utilization. >90% oxygen consumption is used for mitochondria for ATP production.

Increase lactate extraction, decrease ketones, fatty acids and glucose intake.

Septic patients with organ dysfunction can tolerate lower values of oxygen delivery but also reduce cellular oxygen utilization.

>90% oxygen consumption is used for mitochondria for ATP production.

Mitochondrial Dysfunction

Mitochondrial dysfunction Elevated production of NO and superoxide. Increase expression of mitochondrial uncoupling proteins (UCP) Permeability transition pore (PTP): Swelling, proton gradient collapse and cytochome c (Apoptosis)

Elevated production of NO and superoxide.

Increase expression of mitochondrial uncoupling proteins (UCP)

Permeability transition pore (PTP): Swelling, proton gradient collapse and cytochome c (Apoptosis)

Cell Death Hypoxia and Dysoxia. Myocardial cell death is a rare event during sepsis and insufficient to account for the functional depression observed. Reversibility: more functional than anatomical abnormalities.

Hypoxia and Dysoxia.

Myocardial cell death is a rare event during sepsis and insufficient to account for the functional depression observed.

Reversibility: more functional than anatomical abnormalities.

Inflammatory Signaling Endotoxin induced cardiac dysfunction depend on the presence of the cell wall receptors Toll-like receptor 4 and CD14. Toll-like receptor 2 in sepsis by Gram positive. TNFa, IL 1B, Interleulin 6.

Endotoxin induced cardiac dysfunction depend on the presence of the cell wall receptors Toll-like receptor 4 and CD14.

Toll-like receptor 2 in sepsis by Gram positive.

TNFa, IL 1B, Interleulin 6.

Inflammatory Signaling Nitric Oxide (NO): Direct effect on vascular tone, depression on mitochondrial respiration, release of proinflamatory citokines, Antiapoptotic, mitochondrial biogenesis, free radical scanvenger. All three isoforms of NOS are found in cardiomyocytes: NOS1-3 regulate homeostasis and function; NOS2 depress cardiac function.

Nitric Oxide (NO): Direct effect on vascular tone, depression on mitochondrial respiration, release of proinflamatory citokines, Antiapoptotic, mitochondrial biogenesis, free radical scanvenger.

All three isoforms of NOS are found in cardiomyocytes: NOS1-3 regulate homeostasis and function; NOS2 depress cardiac function.

Adrenergic signaling Studies in patients and animals have documented elevated levels of cathecolamines. Prolong and excess stimulation can lead to myocardial damage by calcium overload and cell necrosis Down-regulation of B adrenergic response is associated with high levels of NO

Studies in patients and animals have documented elevated levels of cathecolamines.

Prolong and excess stimulation can lead to myocardial damage by calcium overload and cell necrosis

Down-regulation of B adrenergic response is associated with high levels of NO

Calcium Trafficking

Calcium Trafficking Reductions in Cytosolic calcium levels reduce contractility Is linked with mitochondrial function and integrity To determine time-dependent changes in NO, B adrenergic response and protective effect during prolong sepsis

Reductions in Cytosolic calcium levels reduce contractility

Is linked with mitochondrial function and integrity

To determine time-dependent changes in NO, B adrenergic response and protective effect during prolong sepsis

Conclusions 40%-50% of pt with septic shock develop myocardial depression Cytokines and NO Myocardial depression could protect the heart reducing energy expenditure Further investigation is needed.

40%-50% of pt with septic shock develop myocardial depression

Cytokines and NO

Myocardial depression could protect the heart reducing energy expenditure

Further investigation is needed.

 

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